Maternal vitamin D status in pregnancy and adverse pregnancy outcomes in a group at high risk for pre-eclampsia.

OBJECTIVE: To determine in a group of pregnant women if vitamin D status, based on serum 25-hydroxyvitamin D (25OHD) concentration, was associated with a subsequent risk of pre-eclampsia or adverse pregnancy outcomes. DESIGN: Prospective cohort study. SETTING: Vancouver, British Columbia, Canada (49°N). POPULATION: Women attending a specialist antenatal clinic because of clinical or biochemical risk factors for pre-eclampsia (n = 221). METHODS: Serum 25OHD concentration measured between 10 and 20 weeks of gestation. MAIN OUTCOME MEASURES: Pre-eclampsia and composite adverse pregnancy outcomes. RESULTS: Of the women, 78% were vitamin D insufficient (25OHD <75 nmol/l) and 53% were vitamin D deficient (25OHD <50 nmol/l). There was no difference in the rates of pre-eclampsia, gestational hypertension, preterm birth or composite adverse pregnancy outcomes by 25OHD concentration. CONCLUSIONS: Vitamin D deficiency and insufficiency were common in a group of women at high risk of pre-eclampsia; however, it was not associated with subsequent risk of an adverse pregnancy outcome.

Antioxidant capacity of human milk and its association with vitamins A and E and fatty acid composition.

AIM: The antioxidant capacity of human milk reflects the presence and activity of multiple components, which prevent oxidative rancidity. The aim of this study was to use the Oxygen Radical Absorbance Capacity assay to assess human milk antioxidant capacity and find correlations with milk components. METHODS: Milk samples collected from 60 breastfeeding women at 1 month postpartum were assayed for antioxidant capacity, vitamins E and A, and fatty acids. Potential statistical relationships of concentrations of vitamins A and E and polyunsaturated fatty acids on the antioxidant capacity of human milk were determined. RESULTS: Human milk antioxidant capacity was positively attributed to alpha-tocopherol concentration (rho < 0.05). The vitamin A concentration did not significantly contribute to milk antioxidant capacity, but was correlated to milk alpha-tocopherol concentration (r = 0.587; rho < 0.001). There was no evidence of an inverse relationship between polyunsaturated fatty acids concentration and the antioxidant capacity value of milk. CONCLUSION: This study shows that alpha-tocopherol is an important contributor to the oxidative stability of human milk. Moreover, there was no evidence obtained to show that women who have high levels of milk polyunsaturated fatty acids are predisposed to lower milk antioxidant capacity.

Are plasma homocysteine and methionine elevated when binging and purging behavior complicates anorexia nervosa? Evidence against the transdiagnostic theory of eating disorders.

OBJECTIVE: To determine whether plasma total homocysteine (tHcy) and plasma methionine levels are different in anorexia nervosa restricting type (AN-R) compared to anorexia nervosa binge eating/purging type (AN-BP). METHODS: Cross-sectional design. SUBJECTS: Subjects were recruited from the outpatient program of the Eating Disorders Program at St. Paul's Hospital, Vancouver, Canada. All subjects had a current Diagnostic and Statistical Manual of mental Disorders - Fourth Edition (DSM-IV) AN-R, or AN-BP diagnosis. Controls were recruited from staff and trainees of Child and Family Research Institute, and Children's and Women's Hospital, University of British Columbia. RESULTS: Samples were obtained from AN-R (N=30), AN-BP (N=32) and control women (N=73) and men (N=33). The 5- 95th% confidence intervals from the control women were taken as the normal range. The plasma tHcy and methionine for the control group had a 5-95th percentile range of 5.66-10.57 and 15.3-40.2 microM, respectively. Plasma tHcy was elevated in women with AN-BP (9.24+/-0.85 microM, N=32) but not with AN-R (7.90+/-0.38 microM, N=30). Plasma methionine was decreased in women with AN-BP (22.2+/-1.43 microM, N=32) compared to the control group of women (25.1+/-0.89 microM). The plasma methionine/tHcy ratio was elevated in the women with AN-BP (0.50+/-0.09) but not in those with AN-R (0.34+/-0.03). CONCLUSION: Elevated plasma tHcy and decreased plasma methionine are consistent with impaired homocysteine remethylation. Altered methyl transfer capacity or methyl deficiency could impair monoamine neurotransmitter metabolism potentially impacting cognitive and psychological function.We hypothesize that the treatment of AN-BP should consider the need for nutritional support of methyl metabolism.

The activity of 3-hydroxy-3-methylglutaryl-CoA reductase and acyl-CoA: cholesterol acyltransferase in hepatic microsomes from male, female and pregnant rats. The effect of cholestyramine treatment and the relationship of enzyme activity to microsomal lipid composition.

The relationship of microsomal cholesterol and phospholipid fatty acid composition to the activities of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and acyl-CoA: cholesterol acyltransferase was investigated in male, female virgin and pregnant rats when hepatic cholesterogenesis was stimulated by cholestyramine. Cholestyramine increased HMG-CoA reductase activity in both sexes but had no effect on microsomal free cholesterol level or acyl-CoA: cholesterol acyltransferase activity. The data suggest that during cholestyramine treatment high rates of bile acid synthesis are supported by preferential channelling of cholesterol into this pathway, whilst the substrate pool and activity of acyl-CoA:cholesterol acyltransferase are maintained unaltered. The lack of a consistent relationship among enzyme activities and microsomal lipid composition infers that HMG-CoA reductase and acyl-CoA:cholesterol acyltransferase are regulated in vivo by independent mechanisms which are unlikely to involve modulation by the physical properties of the microsomal lipid.

Perinatal development of hepatic cholesterol synthesis in the rat.

Rates of cholesterol synthesis and HMG CoA reductase activity in rat liver, have been reported to be high before and low after birth. The timing of the decline in perinatal rates of cholesterol synthesis, however, is uncertain. These studies, therefore, determined in vivo rates of cholesterol synthesis using [3H]water and hepatic reductase activity in vitro in perinatal rats. The lipid composition of the plasma, liver and its microsomal subfraction were also determined. Reductase activity increased during late gestation, remained high immediately after birth, then decreased with the commencement of suckling. Rates of cholesterol synthesis increased from gestation day 18 to 20, but in contrast to reductase activity, decreased on the day before birth. Plasma cholesterol and triacylglycerol levels increased to gestation day 19, then decreased to term. By the 6th h after birth, plasma and liver cholesterol and triacylglycerol levels had increased markedly. By 48 h after birth, the high hepatic cholesterol content was associated with an increase in the cholesteryl ester fraction. The microsomal cholesterol/phospholipid molar ratio decreased from gestation day 16 until 12 h after birth, then increased markedly from 36 to 48 h. There was an apparent inverse relationship between the change in microsomal cholesterol/phospholipid molar ratio and the fatty acid unsaturation index from gestation day 16 to 36 h after birth. The results suggest that in late gestation and before suckling, the low in vivo rate of hepatic cholesterol synthesis may not be due to low activity of HMG CoA reductase.

Formula alpha-linolenic (18:3(n - 3)) and linoleic (18:2(n - 6)) acid influence neonatal piglet liver and brain saturated fatty acids, as well as docosahexaenoic acid (22:6(n - 3)).

Saturated fatty acids can be synthesized de novo and play a role in determining properties of structural membranes. The effect of dietary essential fatty acids, linoleic acid (18:2(n - 6)) and alpha-linolenic acid (18:3(n - 3)), on the saturated fatty acid content of membrane phospholipid has not previously been considered in newborn nutrition. The studies report the effect of low (1% fatty acids) or high (4%) formula 18:3(n - 3) with low (16%) or high (30-35%) formula 18:2(n - 6) on the saturated and unsaturated fatty acid composition of liver and brain structural lipid of piglets fed formula from birth for 15 days. A significant inverse relationship between the formula % 18:3(n - 3), but not 18:2(n - 6), and the liver phospholipid palmitic acid (16:0) was found. This may indicate a possible effect of dietary 18:3(n - 3) on de novo synthesis of 16:0 and requires further investigation. Monounsaturated fatty acids in both liver and brain were significantly lower in response to high 18:3(n - 3) and to high 18:2(n - 6) plus low 18:1(n - 9) in the formula. Liver phospholipid and brain total lipid % docosahexaenoic acid (22:6(n - 3)) were significantly higher when formula containing 4% rather than 1% 18:3(n - 3) was fed, suggesting that 1% 18:3(n - 3) may limit tissue (n - 3) fatty acid accretion. These results suggest that future studies of essential fatty acid requirements, specifically 18:3(n - 3), should consider possible influences on the saturated fatty acids which also play a functional role in tissue structural lipids.

Essential fatty acid transfer and fetal development.

Docosahexaenoic acid (22:6n-3) and arachidonic acid (20:4n-6) are important structural components of the central nervous system. These fatty acids are transferred across the placenta, and are accumulated in the brain and other organs during fetal development. Depletion of 22:6n-3 from the retina and brain results in reduced visual function and learning deficits: these may involve critical roles of 22:6n-3 in membrane-dependent signaling pathways and neurotransmitter metabolism. Transfer of 22:6n-3 across the placenta involves specific binding and transfer proteins that facilitate higher concentrations of 22:6n-3 and 20:4n-6, but lower linoleic acid (18:2n-6) in fetal compared with maternal plasma, or in the breast-fed or formula-fed infant. However, human and animal studies both demonstrate that maternal diet impacts fetal 22:6n-3 and 20:4n-6 accretion. After birth, parenteral lipid, human milk and infant formula feeding all result in a marked decrease in plasma 22:6n-3 and 20:4n-6 and an increase in 18:2n-6. Estimation of fetal tissue fatty acid accretion suggests that current preterm infant feeds are unlikely to meet in utero rates of 22:6n-3 accretion. Consideration needs to be given to whether fetal plasma 22:6n-3 and 20:4n-6 enrichment and the low 18:2n-6 facilitates accretion of 22:6n-3 and 20:4n-6 in developing tissues.

Maternal exposure to fish oil primes offspring to harbor intestinal pathobionts associated with altered immune cell balance.

Our previous studies revealed that offspring from rat dams fed fish oil (at 8% and 18% energy), developed impaired intestinal barriers sensitizing the colon to exacerbated injury later in life. To discern the mechanism, we hypothesized that in utero exposure to fish oil, rich in n-3 polyunsaturated fatty acid (PUFA), caused abnormal intestinal reparative responses to mucosal injury through differences in intestinal microbiota and the presence of naïve immune cells. To identify such mechanisms, gut microbes and naïve immune cells were compared between rat pups born to dams fed either n-6 PUFA, n-3 PUFA or breeder chow. Maternal exposure to either of the PUFA rich diets altered the development of the intestinal microbiota with an overall reduction in microbial density. Using qPCR, we found that each type of PUFA differentially altered the major gut phyla; fish oil increased Bacteroidetes and safflower oil increased Firmicutes. Both PUFA diets reduced microbes known to dominate the infant gut like Enterobacteriaceae and Bifidobacteria spp. when compared to the chow group. Uniquely, maternal fish oil diets resulted in offspring showing blooms of opportunistic pathogens like Bilophila wadsworthia, Enterococcus faecium and Bacteroides fragilis in their gut microbiota. As well, fish oil groups showed a reduction in colonic CD8+ T cells, CD4+ Foxp3+ T cells and arginase+ M2 macrophages. In conclusion, fish oil supplementation in pharmacological excess, at 18% by energy as shown in this study, provides an example where excess dosing in utero can prime offspring to harbor intestinal pathobionts and alter immune cell homeostasis.

Hepatic transport of bile salt and bile composition following total parenteral nutrition with and without lipid emulsion in the rat.

The effect of total parenteral nutrition (TPN) on bile flow and composition and on hepatic bile acid transport maximum (Tm) and bile salt-independent bile flow (BSIF) was studied in the rat following seven days TPN containing 33% calories from Intralipid (IL) or Liposyn (LP) or 0% calories from lipid. All TPN regimes markedly reduced bile flow. In no case did TPN cause an increase in bile cholesterol concentration or saturation relative to bile acid and phospholipid. Bile acid Tm was reduced in rats receiving either 0% lipid or 33% IL; BSIF was reduced only in the 0% lipid group. Rats receiving 33% LP had a higher bile flow than the other TPN regimes while bile acid Tm and BSIF were similar to controls. It is proposed that in established TPN, bile flow is reduced largely as a result of decreased hepatic bile acid excretion. In the rat, TPN has no deleterious effect on the molar concentration of cholesterol, phospholipid or bile acid in bile secreted by the hepatocyte. The significant differences between the effect of the two lipid emulsions on hepatobiliary function require further study.

Essential fatty acids in infant nutrition: lessons and limitations from animal studies in relation to studies on infant fatty acid requirements.

Animal studies have been of pivotal importance in advancing knowledge of the metabolism and roles of n-6 and n-3 fatty acids and the effects of specific dietary intakes on membrane composition and related functions. Advantages of animal studies include the rigid control of fatty acid and other nutrient intakes and the degree, timing, and duration of deficiency or excess, the absence of confounding environmental and clinical variables, and the tissue analysis and testing procedures that cannot be performed in human studies. However, differences among species in nutrient requirements and metabolism and the severity and duration of the dietary treatment must be considered before extrapolating results to humans. Studies in rodents and nonhuman primates fed diets severely deficient in alpha-linolenic acid (18:3n-3) showed altered visual function and behavioral problems, and played a fundamental role by identifying neural systems that may be sensitive to dietary n-3 fatty acid intakes; this information has assisted researchers in planning clinical studies. However, whereas animal studies have focused mainly on 18:3n-3 deficiency, there is considerable clinical interest in docosahexaenoic acid (22:6n-3) and arachidonic acid (20:4n-6) supplementation. Information from animal studies suggests that brain and retinal concentrations of 22:6n-3 plateau with 18:3n-3 intakes of approximately 0.7% of energy, but this requirement is influenced by dietary 18:2n-6 intake. Blood and tissue concentrations of 22:6n-3 increase as 22:6n-3 intake increases, with adverse effects on growth and function at high intakes. Animal studies can provide important information on the mechanisms of both beneficial and adverse effects and the pathways of brain 22:6n-3 uptake.

Arachidonic acid concentrations in plasma and liver phospholipid and cholesterol esters of piglets raised on formulas with different linoleic and linolenic acid contents.

The influence of sow milk or infant formulas containing 18:2n-6 and 18:3n-3 (% fatty acids) at 30/1, 16/1, 35/4, or 16/4 on plasma and liver phospholipid (PL) and cholesterol ester (CE) arachidonic acid (20:4n-6) was studied in piglets fed from birth for 15 d. Piglets fed the 35/4, 16/1, and 16/4 formulas had a significantly lower percentage of plasma 20:4n-6 in PL than did piglets fed sow milk or the 30/1 formula. The lowest plasma PL 20:4n-6 was in the 16/4 group, the only group in which liver PL 20:4n-6 was significantly reduced. This suggests competitive inhibition of synthesis or acylation of 20:4n-6 when formula with a high content of 18:3n-3 is fed in conjunction with a low content of 18:2n-6. The percentage of plasma CE 20:4n-6 was not altered by formula feeding. In contrast, the liver CE 20:4n-6 was significantly lower in all formula-fed animals than it was in sow-milk-fed animals. These studies confirm that 20:4n-6 metabolism is altered in artificially fed neonates. Liver and plasma cholesterol concentrations were also significantly lower in all formula-fed than in milk-fed piglets. The potential relationship of the decrease in cholesterol to n-6 fatty acids in CE is unknown.

Infant plasma trans, n-6, and n-3 fatty acids and conjugated linoleic acids are related to maternal plasma fatty acids, length of gestation, and birth weight and length.

BACKGROUND: Arachidonic acid (AA) and docosahexaenoic acid (DHA) are important for growth and neural development. trans Fatty acids (TFAs) may inhibit desaturation of linoleic acid (LA) and alpha-linolenic acid (ALA) to AA and DHA, respectively. Conjugated linoleic acids (CLAs) also alter lipid metabolism and body fat. OBJECTIVE: We determined the associations of birth outcome with maternal and infant plasma concentrations of TFAs, CLAs, AA, and DHA. DESIGN: In healthy women, we sampled maternal blood at 35 wk gestation (n = 58) and umbilical cord blood at birth (n = 70). RESULTS: Mean (+/- SEM) TFA concentrations (% by wt) in infant plasma were as follows: triacylglycerol, 2.83 +/- 0.19 (range: 0.63-12.79); phospholipid, 0.67 +/- 0.03 (0.11-1.33); and cholesteryl ester, 2.04 +/- 0.01 (0.86-4.24). LA, AA, DHA, TFA, and CLA concentrations in infant phospholipids correlated with the same fatty acid in maternal plasma phospholipids (n = 44; P < 0.05). Infant plasma cholesteryl ester and triacylglycerol TFAs and cholesteryl ester CLAs (r = -0.33, -0.42, and -0.49, respectively) were significantly inversely related to length of gestation. Triacylglycerol and cholesteryl ester AA were positively related to length of gestation (r = 0.41 and 0.37, respectively) and birth weight (r = 0.27 and 0.23, respectively). Inverse correlations occurred between infant plasma TFA and DHA concentrations in triacylglycerols (r = -0.33) and between TFA and AA concentrations in cholesteryl esters (r = -0.23). CONCLUSION: The results suggest possible important effects of TFAs and of AA on fetal growth and length of gestation.

Dietary n-3 fatty acid restriction during gestation in rats: neuronal cell body and growth-cone fatty acids.

Growth cones are membrane-rich structures found at the distal end of growing axons and are the predecessors of the synaptic membranes of nerve endings. This study examined whether n-3 fatty acid restriction during gestation in rats alters the composition of growth cone and neuronal cell body membrane fatty acids in newborns. Female rats were fed a standard control diet containing soy oil (8% of fatty acids as 18:3n-3 by wt) or a semisynthetic n-3 fatty acid-deficient diet with safflower oil (0.3% of fatty acids as 18:3n-3 by wt) throughout normal pregnancy. Experiments were conducted on postnatal day 2 to minimize the potential for contamination from synaptic membranes and glial cells. Dietary n-3 fatty acid restriction resulted in lower docosahexaenoic acid (DHA) concentrations and a corresponding higher docosapentaenoic acid concentration in neuronal growth cones, but had no effects on neuronal cell body fatty acid concentrations. These studies suggest that accretion of DHA in growth cones, but not neuronal cell bodies, is affected by n-3 fatty acid restriction during gestation. Differences in other fatty acids or components between the semisynthetic and the standard diet, however, could have been involved in the effects on growth-cone DHA content. The results also provide evidence to suggest that the addition of new membrane fatty acids to neurons during development occurs along the shaft of the axon or at the growth cone, rather than originating at the cell body.

Plasma fatty acid responses, metabolic effects, and safety of microalgal and fungal oils rich in arachidonic and docosahexaenoic acids in healthy adults.

The effect of dietary supplementation with different amounts of a fungal oil containing arachidonic acid (AA, 20:4n--6) and a microalgal oil containing docosahexaenoic acid (DHA, 22:6n--3), blended to give a ratio of AA to DHA of 1.25:1.00, on plasma lipid AA, DHA, cholesterol, and triacylglycerols was evaluated in healthy men. Subjects (n = 8/group) were given 28.8 g fat/d containing 0 x (0 g AA, 0 g DHA), or 1 x (0.8 g AA, 0.6 g DHA), 3 x (2.2 g AA, 1.7 g DHA), or 5 x (3.6 g AA, 2.9 g DHA) the estimated intake of infants fed human milk with 0.5% AA and 0.4% DHA for 14 d. No clinically significant dose-related effects were seen on physical examination or from routine laboratory tests. The microalgal-fungal oil blend resulted in a significant, dose-dependent increase in plasma cholesterol and percentage phospholipid AA and DHA, and a decrease in percentage triacylglycerols and phospholipid linoleic acid. Plasma phospholipid AA and DHA increased approximately 18% and 50%, respectively, with the 1 x dose, similar to that expected at intakes provided by human milk. These oils appear to be safe dietary sources of AA and DHA for healthy adults at intakes equivalent to 0.8 g AA and 0.6 g DHA/d for > or = 2 wk.

Possible biotin deficiency in adults receiving long-term total parenteral nutrition.

Two adult patients receiving total parenteral nutrition on a long-term home basis presented with severe loss of hair. Both patients had extensive gut resection, consumed no biotin orally and received no biotin parenterally. Supplementation with Berroca-C, one ampule containing 200 micrograms biotin per day resulted in gradual regrowth of healthy hair. The patients now receive a parenteral solution containing biotin and have shown no recurrence of alopecia. It is suggested that biotin deficiency can occur in the adult when no preformed biotin is provided to the body and the contribution of this vitamin from intestinal microbial biosynthesis is compromised.

Cholesterol and bile acid synthesis during total parenteral nutrition with and without lipid emulsion in the rat.

The origin of excess plasma free cholesterol known to accumulate in plasma of patients or animals given total parenteral nutrition (TPN) with lipid emulsion was investigated. Rats were infused for 8 days with a specially formulated TPN solution plus either lipid emulsion (lipid-TPN) or an equicaloric volume of 25% dextrose (dextrose-TPN). Laboratory diet-fed controls were sham operated. Lipid-TPN suppressed hepatic HMG CoA reductase (HMG CoAR) activity but elevated cholesterol 7 alpha-hydroxylase (7 alpha-OH) activity. HMG CoAR activity, however, was increased in adipose tissue and skeletal muscle by lipid-TPN when compared to dextrose-TPN. Plasma lecithin/cholesterol acyl transfer activity was similar among all groups. It is suggested that in lipid-TPN excess plasma free cholesterol does not arise from decreased hepatic clearance or plasma esterification but may originate from extrahepatic tissue, possibly through leaching of membrane cholesterol by mesophase phospholipid present in the lipid emulsion. The changes in hepatic HMG CoAR and 7 alpha-OH activity imply that during lipid-TPN plasma free cholesterol is cleared by the liver and catabolized to bile acid.

Plasma lipoprotein fatty acids are altered by the positional distribution of fatty acids in infant formula triacylglycerols and human milk.

BACKGROUND: Triacylglycerol digestion involves hydrolysis of fatty acids esterified at the glycerol 1,3 positions by gastric and pancreatic lipase to produce 2-monoacylglycerols and unesterified fatty acids, which are then absorbed, reesterified to triacylglycerol, and secreted in chylomicrons. Palmitic acid (16:0) is predominantly esterified to the 2 position of human milk triacylglycerol but to the 1,3 positions in the oils used in infant formulas. OBJECTIVE: We aimed to determine whether the position of 16:0 in human milk and infant formula triacylglycerol influences the position of fatty acids in postprandial plasma chylomicron triacylglycerol. DESIGN: Full-term infants were fed formula with 25-27% 16:0 with either 39% of the 16:0(synthesized triacylglycerol) or 6% of the 16:0 (standard formula) esterified at the triacylglycerol 2 position, or were breast-fed (23% 16:0, 81% at the triacylglycerol 2 position) from birth to 120 d of age. Chylomicron fatty acids and plasma lipids were assessed at 30 and 120 d of age. RESULTS: Infants fed the synthesized triacylglycerol formula, standard formula, or breast milk had 15.8%,8.3%, and 28.0% 16:0 in the chylomicron triacylglycerol 2 position (P < 0.05). These results suggest that >/=50% of the dietary triacylglycerol 2-position 16:0 is conserved through digestion, absorption, and chylomicron triacylglycerol synthesis in breast-fed and formula-fed infants. Infants fed the synthesized triacylglycerol formula had significantly lower HDL-cholesterol and apolipoprotein A-I and higher apolipoprotein B concentrations than infants fed the standard formula. CONCLUSION: Dietary triacylglycerol fatty acid distribution may alter lipoprotein metabolism in young infants.

trans Fatty acids in human milk are inversely associated with concentrations of essential all-cis n-6 and n-3 fatty acids and determine trans, but not n-6 and n-3, fatty acids in plasma lipids of breast-fed infants.

BACKGROUND: Human milk fatty acids vary with maternal dietary fat composition. Hydrogenated dietary oils with trans fatty acids may displace cis n-6 and n-3 unsaturated fatty acids or have adverse effects on their metabolism. The effects of milk trans, n-6, and n-3 fatty acids in breast-fed infants are unclear, although n-6 and n-3 fatty acids are important in infant growth and development. OBJECTIVE: We sought to determine the relations between trans and cis unsaturated fatty acids in milk and plasma phospholipids and triacylglycerols of breast-fed infants, and to identify the major maternal dietary sources of trans fatty acids. DESIGN: We collected milk from 103 mothers with exclusively breast-fed 2-mo-old infants, blood from 62 infants, and 3-d dietary records from 21 mothers. RESULTS: Mean (+/-SEM) percentages of trans fatty acids were as follows: milk, 7.1 +/- 0.32%; infants' triacylglycerols, 6.5 +/- 0. 33%; and infants' phospholipids, 3.7 +/- 0.16%. Milk trans fatty acids, alpha-linolenic acid (18:3n-3), arachidonic acid (20:4n-6), docosahexaenoic acid (22:6n-3) (P < 0.001), and linoleic acid (18:2n-6) (P = 0.007) were each related to the same fatty acid in infant plasma phospholipids. Milk trans fatty acids were inversely related to milk 18:2n-6 and 18:3n-3, but not to milk or infant plasma 20:4n-6 or 22:6n-3. trans Fatty acids represented 7.7% of maternal total fat intake (2.5% of total energy); the major dietary sources were bakery products and breads (32%), snacks (14%), fast foods (11%), and margarines and shortenings (11%). CONCLUSIONS: There were comparable concentrations of trans fatty acids in the maternal diet, breast milk, and plasma triacylglycerols of breast-fed infants. Prepared foods were the major dietary source of trans fatty acids.

Effect of a vegetable oil formula rich in linoleic acid on tissue fatty acid accretion in the brain, liver, plasma, and erythrocytes of infant piglets.

The effect of feeding sow-milk formula (SMF) or a vegetable-oil infant formula (FF) with minimal n-6 and n-3 long-chain polyenoic fatty acids (LCPs) but high linoleic acid (18:2n-6) and a high ratio of 18:2n-6 to linolenic acid (18:3n-3) on the fatty acids of brain lipid and liver, plasma, and red cell phospholipids was studied in piglets fed from birth for 5, 10, 15, or 25 d. Compared with SMF, FF reduced the concentrations of 18:1 and n-3 LCPs, especially 22:6n-3, in all tissues and increased 22:4n-6 in brain, liver, plasma, and red cell phosphatidylethanolamine. FF also increased 22:5n-6 in brain lipid, liver, and plasma but not in red cell phospholipids. Thus, changes in tissues capable of in situ desaturation were not completely reflected in the red cell phospholipids. The increased liver and brain n-6 LCP accretion in the FF piglets may suggest competent desaturation and possible inhibition of n-3 desaturation and/or acylation by dietary n-6 fatty acids.

Retina fatty acid composition of piglets fed from birth with a linoleic acid-rich vegetable-oil formula for infants.

The effects of a vegetable-oil-based formula containing 30% 18:2n-6 (18:2 omega-6), 0.8% 18:3n-3, and no n-6 or n-3 long-chain polyunsaturated fatty acids (LCPs) on retina total lipid, ethanolamine phosphoglyceride (EPG), and phosphatidylcholine (PC) fatty acid composition were studied in neonatal piglets. Term-gestation piglets were fed sow milk (SMF) or the formula (FF) from birth for 5, 10, 15, or 25 d. After 25 d feeding, the 22:6n-3 was reduced by 24% in total lipid, 20% in EPG, and 28% in PC of retinas of FF relative to SMF piglets. A compensatory increase in 22:4n-6 and 22:5n-6 concentrations occurred in retina total lipid, EPG, and PC of FF animals. The data suggest that the exclusive feeding of formulas devoid of LCPs and high in 18:2n-6 and/or 18:2n-6 and 18:3n-3 compromises normal accretion of 22:6n-3 in neonatal piglet retina. The potential reversibility of these changes or their effects on vision are not known.