Evaluation of Gastroprotective Activity of Linoleic Acid on Gastric Ulcer in a Mice Model.

BACKGROUND: Gastric ulcer has been a major cause of morbidity and mortality worldwide, and it has been linked to factors such as nutritional deficiency, smoking, stress, and continuous intake of non-steroidal antiinflammatory drugs (NSAIDs). The search for new anti-ulcer therapeutic agents has been the subject of several studies. Recently, the gastroprotective effect of Celtis iguanaea has been reported, with linoleic acid (LA) responsible for many of the therapeutic effects of this medicinal plant. AIMS: This study aims to investigate the gastroprotective activity and the possible mechanisms in which LA may be involved through different experimental assays in mice. METHODS: The gastroprotective activity of LA was evaluated in the ulcer induced by indomethacin, HCl/EtOH, hypothermic-restraint stress and pyloric ligation. For the investigation of gastroprotective mechanisms, the quantification of the volume (mL), pH and total acidity of gastric secretion were considered. RESULTS: The oral administrations of 25 mg/kg, 50 mg/kg or 100 mg/kg of body weight of LA were capable of protecting the gastric mucosa against HCl/ethanol (10 mL/kg p.o.), and oral/intraduodenal treatment administrations of 50 mg/kg LA showed protection from ulcers induced by indomethacin, hypothermic-restraint stress and pyloric ligation. CONCLUSION: The results of this study show the gastroprotective role of LA in gastric mucosal damage induced by all assayed distresses. The observed gastroprotection possibly occurs due to the mediated increase of mucosal defensive factors.

Activation of Autophagy Relieves Linoleic Acid-Induced Inflammation in Large Yellow Croaker (Larimichthys crocea).

High levels of soybean oil (SO) in fish diets enriched with linoleic acid (LA, 18:2n-6) could induce strong inflammation. However, the molecular mechanism underlying LA-induced inflammation in the liver of large yellow croaker (Larimichthys crocea) has not been elucidated. Based on previous research, autophagy has been considered a new pathway to relieve inflammation. Therefore, the present study was performed to investigate the role of autophagy in regulating LA-induced inflammation in the liver of large yellow croaker in vivo and in vitro. The results of the present study showed that activation of autophagy in liver or hepatocytes could significantly reduce the gene expression of proinflammatory factors, such as tumor necrosis factor α (TNFα) and interleukin 1ß (IL1ß). The results of the present study also showed that inhibition of autophagy could upregulate the gene expression of proinflammatory factors and downregulate the gene expression of anti-inflammatory factors in vivo and in vitro. Furthermore, autophagy could alleviate LA-induced inflammatory cytokine gene expression in vivo and in vitro, while inhibition of autophagy obtained the opposite results. In conclusion, our study shows that autophagy could regulate inflammation and alleviate LA-induced inflammation in the liver of large yellow croaker in vivo and in vitro for the first time, which may offer considerable benefits to the aquaculture industry and human health.

Activation of the Farnesoid X Receptor (FXR) Suppresses Linoleic Acid-Induced Inflammation in the Large Yellow Croaker (Larimichthys crocea).

BACKGROUND: High linoleic acid (LA) intake leads to inflammation that adversely influences health in fish. However, whether the farnesoid X receptor (FXR) could be an effective target for regulating LA-induced inflammation remains unknown. OBJECTIVE: The purpose of this study was to investigate the role of FXR in the regulation of LA-induced inflammation in large yellow croakers. METHODS: Large yellow croakers (initial weight of 10.03 ± 0.02 g) were allocated to 4 groups and fed a fish oil diet (6% FO), a soybean oil diet (6% SO), or the SO diet supplemented with 300 or 900 mg chenodeoxycholic acid (CDCA)/kg for 10 wk. The cultured kidney cell line PCK and primary hepatocytes from large yellow croakers were stimulated by LA (50 µM) after pretreatment with an FXR ligand (GW4064 or CDCA) or transfection with fxr-small interfering RNA (siFXR). mRNA expression of proinflammatory genes in the head kidney and liver tissues, PCK cells, and primary hepatocytes was determined by qPCR. The luciferase reporter assay, electrophoretic mobility shift assay, and immunoprecipitation assay were conducted in HEK 293T cells to determine the transcriptional activity of P65 and protein interactions between P65 and FXR or the small heterodimer partner (SHP). RESULTS: Proinflammatory genes were 93-1180% higher in the SO group compared with the FO group. CDCA supplementation decreased mRNA expression of proinflammatory genes by 17-87% while increasing fxr and shp expression by 120-460%. In PCK cells and primary hepatocytes, ligand-mediated activation of FXR decreased the LA-induced expression of proinflammatory genes by 18-67%, whereas siRNA-mediated knockdown of FXR increased the LA-induced expression of proinflammatory genes by 64-96%. FXR bound to the promoter of shp and regulated its mRNA expression. Both FXR and SHP could bind to P65 to suppress the transcriptional activity of P65. CONCLUSIONS: These results indicate that FXR has anti-inflammatory properties in large yellow croakers by directly and indirectly suppressing NFκB activity.

Dysregulation of Hypothalamic Gene Expression and the Oxytocinergic System by Soybean Oil Diets in Male Mice.

Soybean oil consumption has increased greatly in the past half-century and is linked to obesity and diabetes. To test the hypothesis that soybean oil diet alters hypothalamic gene expression in conjunction with metabolic phenotype, we performed RNA sequencing analysis using male mice fed isocaloric, high-fat diets based on conventional soybean oil (high in linoleic acid, LA), a genetically modified, low-LA soybean oil (Plenish), and coconut oil (high in saturated fat, containing no LA). The 2 soybean oil diets had similar but nonidentical effects on the hypothalamic transcriptome, whereas the coconut oil diet had a negligible effect compared to a low-fat control diet. Dysregulated genes were associated with inflammation, neuroendocrine, neurochemical, and insulin signaling. Oxt was the only gene with metabolic, inflammation, and neurological relevance upregulated by both soybean oil diets compared to both control diets. Oxytocin immunoreactivity in the supraoptic and paraventricular nuclei of the hypothalamus was reduced, whereas plasma oxytocin and hypothalamic Oxt were increased. These central and peripheral effects of soybean oil diets were correlated with glucose intolerance but not body weight. Alterations in hypothalamic Oxt and plasma oxytocin were not observed in the coconut oil diet enriched in stigmasterol, a phytosterol found in soybean oil. We postulate that neither stigmasterol nor LA is responsible for effects of soybean oil diets on oxytocin and that Oxt messenger RNA levels could be associated with the diabetic state. Given the ubiquitous presence of soybean oil in the American diet, its observed effects on hypothalamic gene expression could have important public health ramifications.

Effects of Cyclic Fatty Acid Monomers from Heated Vegetable Oil on Markers of Inflammation and Oxidative Stress in Male Wistar Rats.

This study assesses the effects of cyclic fatty acid monomers (CFAM) from heated vegetable oils on oxidative stress and inflammation. Wistar rats were fed either of these four diets for 28 days: canola oil (CO), canola oil and 0.5% CFAM (CC), soybean oil (SO), and soybean oil and 0.5% CFAM (SC). Markers of oxidative stress and inflammation were determined by micro liquid chromatography tandem mass spectrometry (micro-LC-MS/MS) and enzyme-linked immunosorbent assay (ELISA) kits, respectively. Analysis of variance (ANOVA) for a 2 × 2 factorial design was performed to determine the CFAM and oil effects and interactions between these two factors at P ≤ 0.05. For significant interactions, a post hoc multiple comparison test was performed, i.e., Tukey HSD (honest significant difference) test. CFAM induced higher plasma levels of 15-F2t-IsoP (CC, 396 ± 43 ng/mL, SC, 465 ± 75 ng/mL vs CO, 261 ± 23 ng/mL and SO, 288 ± 35 ng/mL, P < 0.05). Rats fed the SC diet had higher plasma 2,3-dinor-15-F2t-IsoP (SC, 145 ± 9 ng/mL vs CC, 84 ± 8 ng/mL, CO, 12 ± 1 ng/mL, and SO, 12 ± 1 ng/mL, P < 0.05), urinary 2,3-dinor-15-F2t-IsoP (SC, 117 ± 12 ng/mL vs CC, 67 ± 13 ng/mL, CO, 15 ± 2 ng/mL, and SO, 18 ± 4 ng/mL, P < 0.05), and plasma IL-6 (SC, 57 ± 10 pg/mL vs CC, 48 ± 11 pg/mL, CO, 46 ± 9 pg/mL, and SO, 44 ± 4 pg/mL, P < 0.05) than the other three diet groups. These results indicate that CFAM increased the levels of markers of oxidative stress, and those effects are exacerbated by a CFAM-high-linoleic acid diet.

Neither linoleic acid nor arachidonic acid promote white adipose tissue inflammation in Fads2-/- mice fed low fat diets.

Dietary n-6 polyunsaturated fatty acids (PUFA) are widely perceived to promote inflammation and contribute to the development of chronic diseases. This dogma has been recently questioned due to evidence that n-6 PUFA, specifically linoleic acid (LA, 18:2n-6) and arachidonic acid (AA, 20:4n-6), do not appear to activate inflammatory signalling pathways when consumed in moderate amounts. However, delineating the independent roles of different dietary n-6 PUFA in vivo is challenging because LA is continuously converted into AA in a pathway regulated by the fatty acid desaturase 2 (Fads2) gene. The objective of this study was to investigate the independent roles of LA and AA on white adipose tissue (WAT) inflammatory signalling pathways using Fads2-/- mice. We hypothesized that dietary LA would not induce WAT inflammation, unless it was endogenously converted into AA. Male C57BL/6 wild-type (WT) and Fads2-/- mice were fed low-fat isocaloric diets containing either 7% corn oil w/w (CD, containing ~42% LA) or 7% ARASCO oil w/w (AD, containing ~27% AA) for 9 weeks. WAT inflammatory gene expression, protein levels, as well as phospholipid (PL) and triacylglycerol (TAG) fatty acid composition, were analyzed by RT-qPCR, western blots, and gas chromatography, respectively. Fads2-/- mice fed CD had high LA, but little-to-no GLA (18:3n-6), DGLA (20:3n-6), and AA in PLs and TAGs compared to their WT counterparts. In comparison, Fads2-/- and WT mice fed AD showed minimal differences in n-6 PUFA content in serum and WAT, despite having significantly more AA than CD-fed mice. No differences in gene expression for common inflammatory adipokines (e.g. Mcp-1, Ccl5, Tnfα) or key regulators of eicosanoid production (e.g. Cox-2, Alox-12, Alox-15) were detected in WAT between any of the diet and genotype groups. Furthermore, no differences in MCP-1, and total or phosphorylated STAT3 and p38 inflammatory proteins, were observed. Collectively, these results demonstrate that neither LA nor AA promote WAT inflammation when consumed as part of a low-fat diet. Therefore, the existing dogma surrounding n-6 PUFA and inflammation needs to be reconsidered.

Good Fats versus Bad Fats: A Comparison of Fatty Acids in the Promotion of Insulin Resistance, Inflammation, and Obesity.

Recently, debate has erupted in both the scientific community and throughout the lay public around whether a low-fat or low-carbohydrate diet is better for weight loss. In other words, is it better to cut fat or cut carbohydrate for weight loss. However, going beyond this debate (fat versus carbohydrate), are questions around whether certain fatty acids are worse for promoting insulin resistance, inflammation, and obesity. The overall evidence in the literature suggests that medium-chain saturated fats (such as lauric acid, found in coconut oil) and monounsaturated fat (oleic acid, found in olive oil) are less likely to promote insulin resistance, inflammation, and fat storage compared to long-chain saturated fatty acids (such as stearic acid found in large quantities in butter, but particularly palmitic acid found in palm oil) especially when consumed on top of a diet moderate in refined carbohydrates. Compared to long-chain saturated fats, lauric acid and oleic acid have an increased fatty acid oxidation rate, are more likely to be burned for energy and less likely to be stored in adipose tissue, and thus promote increased energy expenditure. Omega-6 polyunsaturated fatty acids (PUFAs), such as linoleic acid, as found in vegetable oils may contribute to obesity, whereas omega-3 PUFA may be protective. Importantly, both olive oil as part of a Mediterranean diet, and omega-3 from fish and fish oil have been proven to reduce risk of cardiovascular (CV) events.

Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse.

A significant change in the Western diet, concurrent with the obesity epidemic, was a substitution of saturated fatty acids with polyunsaturated, specifically linoleic acid (LA). Despite increasing investigation on type as well as amount of fat, it is unclear which fatty acids are most obesogenic. The objective of this study was to determine the obesogenic potency of LA vs. saturated fatty acids and the involvement of hypothalamic inflammation. Forty-eight mice were divided into four groups: low-fat or three high-fat diets (HFDs, 45% kcals from fat) with LA comprising 1%, 15% and 22.5% of kilocalories, the balance being saturated fatty acids. Over 12 weeks, bodyweight, body composition, food intake, calorimetry, and glycemia assays were performed. Arcuate nucleus and blood were collected for mRNA and protein analysis. All HFD-fed mice were heavier and less glucose tolerant than control. The diet with 22.5% LA caused greater bodyweight gain, decreased activity, and insulin resistance compared to control and 1% LA. All HFDs elevated leptin and decreased ghrelin in plasma. Neuropeptides gene expression was higher in 22.5% HFD. The inflammatory gene Ikk was suppressed in 1% and 22.5% LA. No consistent pattern of inflammatory gene expression was observed, with suppression and augmentation of genes by one or all of the HFDs relative to control. These data indicate that, in male mice, LA induces obesity and insulin resistance and reduces activity more than saturated fat, supporting the hypothesis that increased LA intake may be a contributor to the obesity epidemic.

Reducing dietary intake of linoleic acid of mouse dams during lactation increases offspring brain n-3 LCPUFA content.

Omega (n-)3 and n-6 long chain polyunsaturated fatty acids (LCPUFA) accumulation in the infant brain after birth is strongly driven by dietary supply of n-3 and n-6 LCPUFAs and their C18 precursors through breast milk or infant formula. n-3 LCPUFA accretion is associated with positive effects on neurodevelopmental outcome whereas high n-6 LCPUFA accumulation is considered disadvantageous. Maternal diet is crucial for breast milk fatty acid composition. Unfortunately, global increases in linoleic acid (C18:2n-6; LA) intake have dramatically increased n-6 LCPUFA and reduced n-3 LCPUFA availability for breastfed infants. We investigated the effects of reducing maternal dietary LA, or increasing n-3 LCPUFA, during lactation on milk and offspring brain fatty acids in mice. Offspring brain n-3 LCPUFA was higher following both interventions, although effects were mediated by different mechanisms. Because of competitive interactions between n-3 and n-6 fatty acids, lowering maternal LA intake may support neurodevelopment in breastfed infants.

Omega-3 PUFAs Lower the Propensity for Arachidonic Acid Cascade Overreactions.

A productive view of the benefits from omega-3 (n-3) nutrients is that the dietary essential omega-6 (n-6) linoleic acid has a very narrow therapeutic window which is widened by n-3 nutrients. The benefit from moderate physiological actions of the arachidonic acid cascade can easily shift to harm from excessive pathophysiological actions. Recognizing the factors that predispose the cascade to an unwanted overactivity gives a rational approach for arranging beneficial interactions between the n-3 and n-6 essential nutrients that are initial components of the cascade. Much detailed evidence for harmful cascade actions was collected by pharmaceutical companies as they developed drugs to decrease those actions. A remaining challenge is to understand the factors that predispose the cascade toward unwanted outcomes and create the need for therapeutic interventions. Such understanding involves recognizing the similar dynamics for dietary n-3 and n-6 nutrients in forming the immediate precursors of the cascade plus the more vigorous actions of the n-6 precursor, arachidonic acid, in forming potent mediators that amplify unwanted cascade outcomes. Tools have been developed to aid deliberate day-to-day quantitative management of the propensity for cascade overactivity in ways that can decrease the need for drug treatments.

The association between linoleic acid levels in colostrum and child cognition at 2 and 3 y in the EDEN cohort.

BACKGROUND: Breastfeeding has been associated with improved cognitive development. This may be explained by polyunsaturated fatty acid (PUFA) content of breast milk, especially long-chain (LC) PUFA that are needed for postnatal brain growth. METHODS: Using data from the French EDEN cohort, we aimed to study whether the PUFA content of colostrum may explain observed associations between breastfeeding duration and cognitive scores at 2 and 3 y. A total of 709 breastfed children with available data on PUFA composition of milk were assessed using parent-reported questionnaires for motor and language at 2 y of age, or global cognition at 3 y. Multiple linear regressions were used to examine associations between PUFA levels and child cognitive scores, after controlling for many confounders. RESULTS: We found no association between LCPUFA levels in colostrum and child development. However, levels of linoleic acid (LA) were negatively associated with motor and cognitive scores, independently of breastfeeding duration. Children breastfed with the highest levels of LA tended to score closer to the never breastfed children than children breastfed with the lowest levels of LA. CONCLUSION: Our findings suggest that too high levels of LA in colostrum are associated with poorer child development at 2 and 3 y.

Bats and zoonotic viruses: can we confidently link bats with emerging deadly viruses?

An increasingly asked question is 'can we confidently link bats with emerging viruses?'. No, or not yet, is the qualified answer based on the evidence available. Although more than 200 viruses - some of them deadly zoonotic viruses - have been isolated from or otherwise detected in bats, the supposed connections between bats, bat viruses and human diseases have been raised more on speculation than on evidence supporting their direct or indirect roles in the epidemiology of diseases (except for rabies). However, we are convinced that the evidence points in that direction and that at some point it will be proved that bats are competent hosts for at least a few zoonotic viruses. In this review, we cover aspects of bat biology, ecology and evolution that might be relevant in medical investigations and we provide a historical synthesis of some disease outbreaks causally linked to bats. We provide evolutionary-based hypotheses to tentatively explain the viral transmission route through mammalian intermediate hosts and to explain the geographic concentration of most outbreaks, but both are no more than speculations that still require formal assessment.

Fatty acid composition, physicochemical properties, antioxidant and cytotoxic activity of apple seed oil obtained from apple pomace.

BACKGROUND: Apple pomace is generated in huge quantities in juice-processing industries the world over and continuous efforts are being made for its inclusive utilization. In this study, apple seeds separated from industrial pomace were used for extraction of oil. The fatty acid composition, physicochemical and antioxidant as well as in vitro anticancer properties of extracted oil were studied to assess its suitability in food and therapeutic applications. RESULTS: The fatty acid composition of seed oil revealed the dominance of oleic (46.50%) and linoleic acid (43.81%). It had high iodine (121.8 g I 100 g⁻¹) and saponification value (184.91 mg KOH g⁻¹ oil). The acid value, refractive index and relative density were 4.28 mg KOH g⁻¹, 1.47 and 0.97 mg mL⁻¹, respectively. The antioxidant potential (IC50) of apple seed oil was 40.06 µg mL⁻¹. Cytotoxicity of apple seed oil against CHOK1, SiHa and A549 cancer cell lines ranged between 0.5 ± 0.06% and 88.6 ± 0.3%. CONCLUSION: The physicochemical properties of apple seed oil were comparable with edible food oil, indicating its better stability and broad application in the food and pharmaceutical industries. Apple seed oil could be a good source of natural antioxidants. Also, the in vitro cytotoxic activity against specific cell lines exhibited its potential as an anticancer agent.

Effects of trans-fatty acids on liver lipid metabolism in mice fed on diets showing different fatty acid composition.

AIM: Our aim was to investigate the effects of trans-fatty acids (TFA) on liver lipid metabolism in mice fed on experimental diets rich in either oleic or linoleic acid. METHODS: Twenty-two male CF1 mice (22.0 ± 0.1 g) were fed with diets rich in corn oil or olive oil, supplemented or not with TFA (0.75 g TFA/100 g diet), for 4 weeks. Changes in triacylglycerol content, the activity and expression of enzymes involved in lipogenesis and fatty acid oxidation were measured. RESULTS: Supplementation of an olive oil-rich diet with TFA increased liver triacylglycerols, the activity and expression of lipogenic enzymes and sterol regulatory element-binding protein SREBP-1a expression. By contrast, when TFA were added to a corn oil-rich diet, they did not modify these parameters. No significant differences were observed among the experimental groups in the activity and expression of carnitine palmitoyltransferase-Ia, body and liver weights or serum triacylglycerol concentrations. CONCLUSIONS: The effect of TFA on liver fat accumulation depends on the dietary fatty acid composition. Steatosis induced by TFA when included in an olive oil diet (but not in a corn oil diet) was associated with an increased lipogenesis but not with a decreased fatty acid oxidation in animals fed on the olive oil diet. This metabolic change is mediated by SREBP-1a but not by SREBP-1c, and seems to be independent of insulin.

Trans fatty acids and cardiovascular health: research completed?

This review asks the question if further research on trans fatty acids and cardiovascular health is needed. We therefore review the evidence from human studies on trans fatty acids and cardiovascular health, and provide a quantitative review of effects of trans fatty acid intake on lipoproteins. The results show that the effect of industrially produced trans fatty acids on heart health seen in observational studies is larger than predicted from changes in lipoprotein concentrations. There is debate on the effect of ruminant trans fatty acids and cardiovascular disease. Of special interest is conjugated linoleic acid (CLA), which is produced industrially for sale as supplements. Observational studies do not show higher risks of cardiovascular disease with higher intakes of ruminant trans fatty acids. However, CLA, industrial and ruminant trans fatty acids all raise plasma low-density lipoprotein and the total to high-density lipoprotein ratio. Gram for gram, all trans fatty acids have largely the same effect on blood lipoproteins. In conclusion, the detrimental effects of industrial trans fatty acids on heart health are beyond dispute. The exact size of effect will remain hard to determine. Further research is warranted on the effects of ruminant trans fatty acids and CLA on cardiovascular disease and its risk factors.

Docosahexaenoic acid synthesis from alpha-linolenic acid is inhibited by diets high in polyunsaturated fatty acids.

The conversion of the plant-derived omega-3 (n-3) α-linolenic acid (ALA, 18:3n-3) to the long-chain eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3) can be increased by ALA sufficient diets compared to ALA deficient diets. Diets containing ALA above an optimal level result in no further increase in DHA levels in animals and humans. The present study evaluates means of maximizing plasma DHA accumulation by systematically varying both linoleic acid (LA, 18:2n-6) and ALA dietary level. Weanling rats were fed one of 54 diets for three weeks. The diets varied in the percentage of energy (en%) of LA (0.07-17.1 en%) and ALA (0.02-12.1 en%) by manipulating both the fat content and the balance of vegetable oils. The peak of plasma phospholipid DHA (>8% total fatty acids) was attained as a result of feeding a narrow dietary range of 1-3 en% ALA and 1-2 en% LA but was suppressed to basal levels (∼2% total fatty acids) at dietary intakes of total polyunsaturated fatty acids (PUFA) above 3 en%. We conclude it is possible to enhance the DHA status of rats fed diets containing ALA as the only source of n-3 fatty acids but only when the level of dietary PUFA is low (<3 en%).

Dietary linoleic acid elevates endogenous 2-arachidonoylglycerol and anandamide in Atlantic salmon (Salmo salar L.) and mice, and induces weight gain and inflammation in mice.

Dietary intake of linoleic acid (LA) has increased dramatically during the twentieth century and is associated with a greater prevalence of obesity. Vegetable oils are recognised as suitable alternatives to fish oil (FO) in feed for Atlantic salmon (Salmo salar L.) but introduce high amounts of LA in the salmon fillet. The effect on fish consumers of such a replacement remains to be elucidated. Here, we investigate the effect of excessive dietary LA from soyabean oil (SO) on endocannabinoid levels in Atlantic salmon and mice, and study the metabolic effects in mice when SO replaces FO in feed for Atlantic salmon. Atlantic salmon were fed FO and SO for 6 months, and the salmon fillet was used to produce feed for mice. Male C57BL/6J mice were fed diets of 35% of energy as fat based on FO- and SO-enriched salmon for 16 weeks. We found that replacing FO with SO in feed for Atlantic salmon increased LA, arachidonic acid (AA), decreased EPA and DHA, elevated the endocannabinoids 2-arachidonoylglycerol (2-AG) and anandamide (AEA), and increased TAG accumulation in the salmon liver. In mice, the SO salmon diet increased LA and AA and decreased EPA and DHA in the liver and erythrocyte phospholipids, and elevated 2-AG and AEA associated with increased feed efficiency, weight gain and adipose tissue inflammation compared with mice fed the FO salmon diet. In conclusion, excessive dietary LA elevates endocannabinoids in the liver of salmon and mice, and increases weight gain and counteracts the anti-inflammatory properties of EPA and DHA in mice.

A.S.P.E.N. position paper: Clinical role for alternative intravenous fat emulsions.

The currently available, standard soybean oil (SO)-based intravenous fat emulsions (IVFEs) meet the needs of most parenteral nutrition (PN) patients. There are alternative oil-based fat emulsions, such as medium-chain triglycerides (MCTs), olive oils (OOs), and fish oils (FOs), that, based on extensive usage in Europe, have an equivalent safety profile to SO. These alternative IVFEs are metabolized via different pathways, which may lead to less proinflammatory effects and less immune suppression. These alternative oil-based IVFEs are not currently available in the United States. Many patients who require IVFEs are already in a compromised state. Such patients could potentially have better clinical outcomes when receiving one of the alternative IVFEs to diminish the intake of the potentially proinflammatory ω-6 fatty acid-linoleic acid-which comprises more than 50% of the fatty acid profile in SO. Further research is needed on these alternative oil-based IVFEs to identify which IVFE oils or which combination of oils may be most clinically useful for specific patient populations.

Anticancer effects of garlic and garlic-derived compounds for breast cancer control.

Garlic and garlic-derived compounds reduce the development of mammary cancer in animals and suppress the growth of human breast cancer cells in culture. Oil-soluble compounds derived from garlic, such as diallyl disulfide (DADS), are more effective than water-soluble compounds in suppressing breast cancer. Mechanisms of action include the activation of metabolizing enzymes that detoxify carcinogens, the suppression of DNA adduct formation, the inhibition of the production of reactive oxygen species, the regulation of cell-cycle arrest and the induction of apoptosis. Selenium-enriched garlic or organoselenium compounds provide more potent protection against mammary carcinogenesis in rats and greater inhibition of breast cancer cells in culture than natural garlic or the respective organosulfur analogues. DADS synergizes the effect of eicosapentaenoic acid, a breast cancer suppressor, and antagonizes the effect of linoleic acid, a breast cancer enhancer. Moreover, garlic extract reduces the side effects caused by anti-cancer agents. Thus, garlic and garlic-derived compounds are promising candidates for breast cancer control.

The influence of short-chain essential fatty acids on children with attention-deficit/hyperactivity disorder: a double-blind placebo-controlled study.

Essential fatty acids (EFA) are needed for normal sensory, cognitive, and motor function. The EFA blood profile seems to be different in children with attention-deficit/hyperactivity disorder (ADHD) as compared to matched controls. Previous open EFA supplementation trials were successful in demonstrating significant therapeutic effects in this population, whereas most of the randomized controlled trials failed to show any benefit over placebo. The current randomized, double-blind, placebo-controlled trial tested the influence of short-chain EFA supplementation on ADHD children, using parent and teacher questionnaires and a computerized continuous performance test. A total of 73 unmedicated children aged 7-13 years with a diagnosis of ADHD participated in the study; 63 children completed the study. The EFA supplement contained 480 mg of linoleic acid and 120 mg of alpha-linolenic acid, and the placebo contained 1000 mg of vitamin C (daily amounts); both were given for a 7-week supplementation period. Analysis of variance for repeated measures revealed that both treatments ameliorated some of the symptoms, but no significant differences were found between the groups in any of the treatment effects.