[Essential fatty acids and dermatoses; preliminary note].
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Fatty Acids↗
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Essential fatty acid deficiency inhibits early but not late leukocyte infiltration in rabbit myocardial infarcts.
Essential fatty acid (EFA) deficiency, induced by elimination of the dietary (n-6) fatty acids, has been shown to limit inflammatory cell influx and consequent enhanced eicosanoid production in experimental glomerulonephritis and hydronephrosis. To determine whether EFA-deficiency exerts anti-inflammatory effects following left ventricular myocardial infarction (LVMI), male weanling rabbits were fed EFA-deficient diet for 3 months prior to 60 minutes of distal left circumflex coronary artery occlusion followed by reperfusion. One and 4 days later, corresponding to infiltration of cardiac tissue with polymorphonuclear (PMN) and mononuclear leukocytes respectively, infarcted hearts were buffer perfused and stimulated to produce eicosanoids with f-met-leu-phe or bradykinin. One day following LVMI, the hearts of EFA-deficient rabbits demonstrated a marked suppression of PMN infiltration and eicosanoid production relative to controls. Four days following myocardial infarction, no differences were observed in mononuclear cell invasion, collagen deposition, or eicosanoid production between EFA-deficient and normal hearts. Our data show that EFA-deficiency inhibits PMN influx and consequent enhanced eicosanoid production without affecting the later appearance of mononuclear cells, collagen deposition, or eicosanoid production. Recent studies have shown that suppression of PMN invasion limits the extent of tissue damage following LVMI. Selective inhibition of PMN infiltration is possible and may be useful in the management of acute myocardial infarction.
6-Ketoprostaglandin F1 alpha↗
Essential fatty acids and prostaglandins.
The World Health Organization's recommendation for dietary intake of essential fatty acids is 3% of energy (en%) of linoleate. Evidence from rat studies suggests that more than 3 en% is desirable for the regulation of eicosanoid metabolism. With such a low level of available linoleate, humans tend to synthesize more prostanoids than they do with 6% or more energy from linoleate. High rates of prostanoid synthesis probably are deleterious, so that the lower rate commensurate with 6-12 en% of linoleate probably is desirable. The amount of linoleate needed for normal function is influenced by the dietary content of other fatty acids, particularly saturated fats and those of the n-3 family. Vitamin E is necessary for normal metabolism of polyunsaturated fatty acids. In a diet providing sufficient available total energy with 30% as fat, the lower range of linoleate (6-8 en%) probably is sufficient if the saturated fatty acid content is 10% or less. With a greater proportion of saturated fatty acids, more linoleate is needed to maintain a polyunsaturated to saturated fatty acid ratio of 0.7 to 1.0. Some n-3 fatty acids probably are required, and more than a minimal amount may be beneficial. Current recommendations are for 0.5-1.0 en% in a diet containing 5-6 en% of linoleate.
Adolescent↗
Effectiveness of dietary essential fatty acid deficiency in development of a model of endogenous renal prostaglandin deficiency.
An essential fatty acid deficient diet (EFAD) was administered to rats to determine the feasibility of using a model of endogenous arachidonic acid deficiency to study the role of prostaglandins in the kidney. Beginning at weaning rats were fed a diet containing less than 0.2% linoleic acid. Prostaglandin E (PGE) production was determined in vitro by stimulation of renal papillary slices with 1500 mOsm NaCl in Krebs-Henseleit buffer and in vivo by 24 hour urine collection. EFAD caused a reduction of arachidonic acid in the renal papilla to 13% of levels in control rats (P less than .0005). In vitro PGE release from incubated papillae of EFAD rats was barely detectable at baseline but increased with stimulation to approximately 50% of PGE levels observed in normal tissues. Urinary PGE, volume and sodium excretion were not significantly different between EFAD and control rats. These results suggest that despite significant differences in arachidonic acid stores between EFAD and normal rats, the usefulness of this animal model to study prostaglandin-mediated events may be limited by the residual capacity of the EFAD papilla to produce prostaglandin.
Animals↗
Use of a fish oil-based lipid emulsion to treat essential fatty acid deficiency in a soy allergic patient receiving parenteral nutrition.
The treatment of essential fatty acid deficiency (EFAD) in a 17-year-old male following allogeneic bone marrow transplantation is described. His transplant was complicated by gastrointestinal bleeding that precluded the use of enteral feedings. Due to a severe soy allergy, he could not tolerate any intravenous fat emulsions marketed in the US. After months of receiving fat-free parenteral nutrition and intermittent use of enteral feeds, he developed signs and symptoms consistent with EFAD, including a rash and an elevated plasma triene:tetraene ratio of 0.231 (0.013-0.05). After receiving FDA approval, a parenteral fish oil emulsion was administered to provide fat calories and sufficient alpha-linolenic and linoleic acid to correct his EFAD. Therapy was initiated at 0.2 g/kg/day and advanced to 0.67 g/kg/day, providing approximately 45 mg/kg/day of linoleic acid. After 10 days of therapy, his rash disappeared and his triene:tetraene ratio improved to 0.07. By day 17 the ratio normalized to 0.047. This suggests that using a fish oil emulsion with minimal linoleic acid may be safely used as the sole source of fat calories and may be an option to prevent or treat EFAD in subjects allergic to soy that require a parenteral source of fat.
Adolescent↗
Analysis of the intestinal absorption of essential fatty acids in vivo in the rat.
The absorption and competition kinetics of the essential fatty acids (EFAs), linoleic acid (LA), alpha-linolenic acid (alphaLnA) and arachidonic acid (AA) in vivo were studied in the perfused rat jejunum. Uptake of each EFA on its own followed saturable kinetics at low luminal concentrations, suggesting a facilitative transport process, the affinity of which increased with chain length and degree of unsaturation. Absorption of one EFA was enhanced by low, whilst competitively inhibited by high, concentrations of a second EFA. Whereas LA and alphaLnA each interfered with the absorption of one another, both had little effect on AA. There was a strong inverse correlation between the relative unsaturation of an EFA and the change in Km of its absorption observed upon inhibition with another EFA. Overall, the results indicated a specific absorptive mechanism, probably involving a transport protein, the affinity of which increased with the degree of unsaturation of the EFA.
Animals↗
Effects of oral supplementation with evening primrose oil for six weeks on plasma essential fatty acids and uremic skin symptoms in hemodialysis patients.
Abnormalities in plasma composition of essential fatty acids (EFAs) may be associated with the etiology of pruritus and other skin problems in patients undergoing hemodialysis. To study whether an oral supplementation with omega-6 (n-6) EFAs would restore deranged plasma EFAs and ameliorate skin symptoms, 9 and 7 dialysis patients were randomly assigned to receive either gamma-linolenic acid (GLA)-rich evening primrose oil (EPO) or linoleic acid (LA) (2 g/day each) for 6 weeks. Plasma concentrations of EFA were analyzed by gas chromatography and uremic skin symptoms were assessed for dryness, pruritus and erythema by questionnaire and visual inspection in a double-blind manner. The patients given EPO exhibited a significant (p < 0.05) increase in plasma dihomo-gamma-linolenic acid (a precursor of anti-inflammatory prostaglandin E1) with no concomitant change in plasma arachidonic acid (a precursor of pro-inflammatory prostaglandin E2 and leukotriene B4). In contrast, those given LA exhibited a significant (p < 0.05) increase in LA but not in any other n-6 EFAs, whereas they exhibited a significant (p < 0.05) decrease in plasma docosahexaenoic acid. The patients given EPO showed a significant (p < 0.05) improvement in the skin scores for the three different uremic skin symptoms over the baseline values and a trend toward a greater improvement (0.05 < p < 0.1) in pruritus scores than those given LA. Results indicate that GLA-rich EPO would be a more favorable supplemental source than LA in terms of shifting eicosanoid metabolism toward a less inflammation status through modifying plasma concentrations of their precursor n-6 EFAs. Further studies are required to confirm the efficacy and safety of EPO therapy for the treatment of uremic pruritus.
Administration, Oral↗
Essential fatty acid status in infants and children with chronic liver disease.
The relationship between essential fatty acid (EFA) status and degree of hyperbilirubinaemia and oxidant stress in infants and children with chronic liver diseases was evaluated. Thirty patients with chronic cholestasis and 30 with liver cirrhosis were examined; 30 healthy subjects served as controls. Patient groups had significant decreases in EFAs and significant elevation of total bilirubin. Levels of thiobarbituric acid reactive substances were significantly raised and were significantly inversely correlated to decreased EFA levels. There were also significant decreases in retinol, alpha-tocopherol and alpha-tocopherol/total lipids ratio, which had significant positive correlations with decreased EFA levels. Infants and children with chronic liver diseases have a high risk of EFA deficiency correlated with progressive elevation of serum bilirubin and progressive deterioration of oxidant status.
Adolescent↗
[Follow-up of essential fatty acids in parenteral nutrition in which a fat preparation is included].
Changes in essential fatty acids of twenty two patients during parenteral nutrition are studied. Two populations (neonatal and others) were differencied. In the neonatal group a percentual decrease in arachidonic acid was showed. In both groups a percentual increase of linoleic acid was observed. Possible implications of these findings are discussed.
Age Factors↗
Protective effects of omega-3 essential fatty acids against formaldehyde-induced neuronal damage in prefrontal cortex of rats.
The aim of this study was to examine the neurotoxicity of formaldehyde on prefrontal cortex and the protective effects of omega-3 essential fatty acids against these toxic effects. For this purpose, 21 male Wistar rats were divided into three groups. The rats in group I comprised the controls, while the rats in group II were injected every other day with formaldehyde (FA). The rats in group III received omega-3 fatty acids daily while exposed to formaldehyde. At the end of the 14-day experimental period, all rats were killed by decapitation. The brains of the rats were removed and the prefrontal cortex tissues were obtained from all brain specimens. Some of the prefrontal cortex tissue specimens were used for determination of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) levels. The remaining prefrontal cortex tissue specimens were used for light microscopic and immunohistochemical evaluation. The levels of SOD and GSH-Px were significantly decreased, and MDA levels were significantly increased in rats treated with formaldehyde compared with those of the controls. Furthermore, in the microscopic examination of this group, formation of apoptotic bodies, pycnotic cells, and apoptotic cells including nuclear fragmentation and membrane budding were observed. However, increased SOD and GSH-Px enzyme activities, and decreased MDA levels were detected in the rats administered omega-3 fatty acids while exposed to formaldehyde. Additionally, cellular damage caused by formaldehyde was decreased, and structural appearance was similar to that of the control rats in this group. The biochemical and histological findings observed in all groups were also confirmed by immunohistochemical evaluation. It was determined that formaldehyde-induced neuronal damage in prefrontal cortex was prevented by administration of omega-3 essential fatty acids.
Animals↗
[Essential fatty acid deficiency in enteral nutrition].
A case is presented of a 57-year-old patient who developed a clinical picture compatible with linoleic acid deficit while on a diet with 6.4 g of this fatty acid (2.8% of total calories). The factors involved in essential fatty acid requirements, and the need of some patients for up to 50 g of linoleic acid in order to reach normal serum levels are discussed. It was concluded that some commercial diets should be supplemented with additional linoleic acid.
Enteral Nutrition↗
Diminished phospholipid incorporation of essential fatty acids in peripheral blood leucocytes from patients with Crohn's disease: correlation with zinc depletion.
Peripheral blood leucocytes from patients with Crohn's disease have been shown to have lower zinc content than those from a normal population. Since zinc influences essential fatty acid metabolism, incorporation of 14C-linoleic and 3H-arachidonic acids was studied in peripheral blood leucocytes from controls and patients with Crohn's disease. The zinc content of the leucocytes was also measured. After incubation for 2 h, content of 3H-arachidonic acid, but not 14C-linoleic acid, was greater in Crohn's disease leucocytes than in controls. In the Crohn's disease leucocytes, incorporation of both labelled fatty acids into the phosphatidylcholine fraction was significantly lower than in controls, whereas the amount of both fatty acids remaining in the leucocytes as free fatty acids was increased by 70%. In Crohn's disease, leucocyte zinc level was positively associated with the percentage of 3H-arachidonic acid incorporation into phosphatidylcholine. We conclude that peripheral blood leucocytes from patients with Crohn's disease have abnormal essential fatty acid metabolism and that 3H-arachidonic acid incorporation into the phosphatidylcholine fraction of leucocyte lipids in Crohn's disease varies as the zinc content of the leucocytes.
Adult↗
The major psychoses and neuroses as omega-3 essential fatty acid deficiency syndrome: substrate pellagra.
Pellagra was once a major cause of three behaviorally different mental disorders-schizophreniform, manic-depressive-like, and phobic neurotic - plus drying dermatoses, autonomic neuropathies, tinnitus, and fatigue. In this preliminary study all three of the corresponding present-day mental diseases are found to exhibit, statistically, the same pellagraform physical disorders but to ameliorate not so much with vitamins as with supplements of a newly discovered trace omega-3 essential fatty acid (w3-EFA), which provides the substrate upon which niacin and other B vitamin holoenzymes act uniquely to form the prostaglandin 3 series tissue hormones regulating neurocircuits en block. Since present-day refining and food selection patterns, as well as pure corn diets, deplete both the B vitamins and W3-EFA, the existence of therapeutically cross-reacting homologous catalyst and substrate deficiency forms of pellagra are postulated, the first contributing to the B vitamin deficiency epidemics of 50-100 years ago, the second to the more recent endemic "Diseases of Western Civilization" which express in certain genetic subgroups as the major mental illnesses of today.
Adult↗
Cytoprotective drugs. Focus on essential fatty acids and sucralfate.
Cytoprotection has been defined as an ability of prostaglandins to prevent gastric mucosal injury produced by a variety of ulcerogenic and necrotizing agents without inhibition of gastric acid secretion or without neutralizing intragastric acidity. Since the first demonstration of cytoprotection by prostaglandins many other agents have been claimed to be cytoprotective. Essential fatty acids: arachidonic and linoleic, licorice products, sucralfate, antacids and sulfhydryl compounds all possess cytoprotective properties. All of these compounds are able to prevent or reduce gastric mucosal necrosis produced by absolute ethanol, a necrotizing agent which injures mucosa independently of the luminal pH. Gastric mucosal protection by essential fatty acids is mediated by their conversion by the gastric mucosa to protective prostaglandins. Sucralfate and antacids are also cytoprotective compounds which stimulate release of endogenous prostaglandins from the gastric mucosa.
Animals↗
Essential fatty acid deficiency in adults receiving total parenteral nutrition.
In seven adult patients receiving fat-free total parenteral nutrition (TPN) for 4 to 8 weeks, weekly determinations of plasma fatty acids and total plasma tocopherols were made. Four patients were deficient in essential fatty acids, as defined by triene: tetraene ratio greater than 0.4, at the end of the second week of TPN. Six patients were deficient by the end of the third week and all seven were deficient by the end of the fifth week of TPN treatment. One patient who was deficient in both essential fatty acids and zinc developed a scaling, eczemoid dermatitis that disappeared within 3 weeks after cessation of TPN and resumption of oral feedings containing both fat and zinc. After resumption of oral feedings by three patients, the triene: tetraene ratio returned to normal within 2 weeks. The mean of total plasma tocopherols fell over a period of 7 weeks and in three individuals, reached levels generally associated with deficiency. There were not any obvious clinical manifestations of vitamin E deficiency.
Adult↗
STUDIES ON ESSENTIAL FATTY ACID DEFICIENCY. EFFECT OF THE DEFICIENCY ON THE LIPIDS IN LIVER MITOCHONDRIA AND OXIDATIVE PHOSPHORYLATION.
1. Dietary deficiency of essential fatty acids results in a twofold increase in the neutral lipid content of liver mitochondria as compared with the corresponding value for stock-fed rats. 2. Deficiency produces changes in the pattern of the constituent fatty acids of the main phospholipid fractions of liver mitochondria which are similar to those previously reported for the lipids of whole liver. There is a fall in the content of C(18:2) acid and to a smaller extent of C(20:4) acid associated with a rise of C(16:1), C(18:1) and C(20:3) acids. 3. Deficiency results in small decreases in the phosphorylation quotients of liver mitochondria during oxidation of succinate and pyruvate, but the values lie within the range reported for normal mitochondria. Mitochondrial respiration with succinate is decreased as a result of deficiency but no change was observed with pyruvate as substrate.
Biochemical Phenomena↗
Essential fatty acids as possible enhancers of the beneficial actions of probiotics.
I investigated whether there is a common link between essential fatty acids and probiotics, which have similar actions and benefits in atopy.I made a critical review of the literature pertaining to the actions of essential fatty acids and probiotics on immune response and the interaction between them with particular reference to atopy.Colonization of the human gastrointestinal tract occurs in the first months and years of life. Probiotics are cultures of beneficial bacteria of healthy gut microflora, which reduce dietary antigen load and thus protect against atopy. A significant reduction in the risk of childhood asthma and other atopic conditions was reported in children who were exclusively breast-fed for at least 4 mo after birth. This beneficial action can be attributed to the immunomodulatory, nutritional, or other components of human milk Human breast milk is rich in long-chain polyunsaturated fatty acids (LCPUFAs), which have immunomodulatory actions. Probiotics and LCPUFAs modulate T-helper 1 and 2 responses, show antibioticlike actions, and alleviate changes related to allergic inflammation. LCPUFAs promote the adhesion of probiotics to mucosal surfaces, which augments the health-promoting effects of probiotics. In view of the similarity in their actions and because LCPUFAs promote the actions of probiotics, I believe that a combination of LCPUFAs and probiotics offer significant protection against atopy. It is likely that breast-feeding and probiotics are two naturally occurring, appropriate events in early human life that have significant health benefits.
Breast Feeding↗
The Canadian Society for Nutritional Sciences 1995 Young Scientist Award Lecture. Recent studies on the synthesis, beta-oxidation, and deficiency of linoleate and alpha-linolenate: are essential fatty acids more aptly named indispensable or conditionally dispensable fatty acids?
Recent research on the synthesis, beta-oxidation, and deficiency of linoleate and alpha-linolenate raises questions about whether the term essential fatty acid is outdated. Linoleate and alpha-linolenate can be synthesized from their respective 16-carbon precursors, which are present in the human diet; whether the rate of conversion and dietary supply of the precursors are sufficient depends on the actual requirement for linoleate and alpha-linolenate. Pure deficiency of linoleate (diet excluding linoleate but including alpha-linolenate and oleate) has not been studied until recently, so it is unclear whether the recommended linoleate intake at 2% of energy, as based on classical essential fatty acid deficiency studies, is appropriate or too high. Despite marked whole-body depletion of linoleate and poor conservation of linoleate stores, pure linoleate deficiency has little effect on growth in rats, suggesting its requirement may be less than 2% of energy. Whole-body fatty acid balance studies indicate that the main route of linoleate and alpha-linolenate metabolism is oxidation, which increases sufficiently that accumulation of dietary linoleate and alpha-linolenate may actually be prevented in undernutrition and fasting refeeding. Part of the oxidized carbon from linoleate and alpha-linolenate is recycled and used for de novo synthesis of "non-essential" fatty acids and cholesterol, which in the brain of the suckling rat, can exceed conversion to longer chain polyunsaturates by as much as 10- to 40-fold. Given the capability to synthesize linoleate and alpha-linolenate, the imprecise knowledge of true linoleate requirement, and the absence of clear symptoms of their deficiency in healthy adults, it might be advantageous to consider using the terms indispensable and conditionally dispensable to clarify the conditional nature of the dietary requirement for linoleate and alpha-linolenate.
Animals↗