Licensed fish-oil concentrate versus cod-liver oil.
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Cod Liver Oil↗
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Mercury and selenium in cod-liver oil.
Cod-liver oil preparations were analyzed for mercury and selenium. The conclusion can be drawn that the intake of mercury and selenium in the normal use of these preparations will be very low.
Capsules↗
[Fatty acid composition and degree of peroxidation in fish oil and cod liver oil preparations].
Omega-3-fatty acids are increasingly used by the selfmedicating patient. Since fish oils in capsules are regarded as dietary food, there are neither official regulations in the Federal Republic of Germany concerning a minimum content of omega-3-fatty acids nor detailed rules for the limitation of autoxidation of these highly reactive substances. Both fatty acid composition and the degree of lipid peroxidation were measured in this study in 23 OTC fish oil preparations. The proportion of omega-3-fatty acids was in most fish oils about 30%; exceptions were the only ethyl ester among the preparations with 59% and the cod liver oils (13% to 22%). Regarding the peroxide value considerable differences were found: the lowest was 2 and the highest was 44.7. Since lipid peroxides and their degradation products are basically toxic, a limitation of the allowed degree of lipid peroxidation in fish oils is strongly recommended.
Animals↗
[Contaminating substances in 22 over-the-counter fish oil and cod liver oil preparations: cholesterol, heavy metals and vitamin A].
Fish oil capsules are increasingly used by self-medicating patients. We studied 22 commercial fish oil and menhaden oil preparations in respect to accompanying substances that could be harmful. The substances measured were: cholesterol as determined by gas liquid chromatography, heavy metals measured by atomic absorption, and vitamin A as determined by high-performance liquid chromatography (HPLC). The contents of cholesterol and heavy metals were in ranges which can be regarded as negligible; the content of vitamin A in menhaden oils, however, was found in amounts which warrant that pregnant women do not exceed the dosage as recommended by the manufacturers.
Animals↗
Extreme decrease of linoleic acid in renal medulla from rats after a diet supplemented with cod liver oil.
Spontaneously hypertensive (SHR) and normotensive rats were fed a diet supplemented with linseed oil or cod liver oil for 22 weeks. The most remarkable finding was an extreme fall of linoleic acid in lipids from renal medulla after cod liver oil supplementation. In free fatty acids (FFA) eicosatrienoic acid (C2): 3n-9) appeared increased as a sign of essential fatty acid (EFA) deficiency.
Animals↗
Beneficial effect of cod liver oil in murine endotoxemia.
Cod liver oil (CLO), a marine fish oil, contains approximately 20% omega-3 fatty acids (OFA). When CLO is administered to humans, inhibition of platelet aggregation, decreased platelet arachidonic acid levels, and reduced levels of endotoxin-induced thromboplastin synthesis by monocytes are observed. Since endotoxin causes both increased platelet aggregation and monocyte generation of thromboplastin with resultant microvascular compromise, the purpose of this study was to determine whether CLO is protective in murine endotoxemia. Swiss Webster mice were given CLO (1.0mg, 10.0mg, or 100mg), or 100mg triolein (an unsaturated fat containing no OFA) or saline (control) intraperitoneally (IP) three hours prior to IP administration of 0.3mg E.coli endotoxin. Survivals at 48 hours post-endotoxin administration were as follows: (A) 1.0mg CLO (4/20, 20%); (B) 10mg CLO (5/20, 25%); (C) 100.0mg CLO (11/20, 55%); (D) 100mg triolein (1/20, 5%); (E) 0.13cc saline (1/20, 5%). The significance of groups A,B,C,D verses the control group E is as follows: A vs E, p = 0.15; B vs E, p = 0.08; C vs E, p = 0.0006; D vs E, p = 0.76. This study demonstrates the beneficial effect of 100mg parenteral CLO in murine endotoxemia. This effect is probably mediated through antiplatelet and/or antimonocyte activating mechanisms.
Animals↗
Reduction in atherosclerosis in swine by cod-liver oil.
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Animals↗
Reduction of intimal hyperplasia in canine autologous vein grafts with cod-liver oil and dipyridamole.
To determine the effects of cod-liver oil and a combination of cod-liver oil and dipyridamole on vein-graft intimal hyperplasia, 76 segments of undistended jugular vein were interposed between bilaterally divided femoral arteries in 38 mongrel dogs who received a 2% cholesterol diet. Ten control animals received the diet alone, 8 received cod-liver oil containing 1.8 g of eicosapentaenoic acid daily 1 week before and for 6 weeks after operation, and 20 dogs received 1.8 g of eicosapentaenoic acid and 75 mg of dipyridamole daily 1 week before and for 6 weeks after operation. A similar and significant (p less than 0.01) increase in serum cholesterol was observed in all three groups. Prothrombin, partial thromboplastin and clotting times and the platelet count were unchanged in the controls and in those receiving cod-liver oil. Clotting time increased in the animals receiving a combination of cod-liver oil and dipyridamole (p less than 0.001). Measurements (406 +/- 27) of intimal thickness were made from each graft. Intimal thickness was 3.7 +/- 0.1 micron before implantation and increased to 78 +/- 8 micron after in the controls. Cod-liver oil limited the increase in intimal thickening, to 24 +/- 3 micron (p less than 0.001); cod-liver oil and dipyridamole further reduced the increase in intimal thickening, to 17 +/- 1.4 micron (p less than 0.001). The data indicate that a combination of cod-liver oil and dipyridamole is more effective than cod-liver oil alone in reducing canine vein-graft intimal hyperplasia (p less than 0.03).
Animals↗
[A bacteriological investigation of Norwegian cod liver oil (author's transl)].
Samples of medicinal cod liver oil collected from four of the main producers in Norway have been investigated for content of microorganism. Viable counts for bacteria and fungi were found to be low. No coliform bacteria, coagulase positive Staphylococcus or Pseudomonas could be detected. The findings suggest that the main part of the flora found in cod liver oil belongs to the family Micrococcaceae. Several of the isolated colonies showed lipolytic activity.
Cod Liver Oil↗
A comparative study between cod liver oil and liquid lard intake on intraocular pressure on rabbits.
Cod liver oil administered intramuscularly (0.2 ml/day) lowered intraocular pressure (IOP) of the rabbit from 21 mmHg to 18 +/- 0.4 mmHg (p less than 0.05 n = 8). A higher dose of cod liver oil (1 ml) further lowered intraocular pressure to 14.5 +/- 0.3 mmHg which remained at this level for up to 80 days when the rabbits were sacrificed. Intramuscular injections of liquid lard did not alter IOP in rabbits. When treatment with cod liver oil was stopped, IOP rose to baseline levels. Topical treatment with cyclooxygenase inhibitors had no effect on the IOP lowering effect of cod liver oil. Topical treatment of rabbit eyes with 1% aspirin solution twice daily (up to 28 days) and flurbiprofen t.i.d. (up to 15 days) caused no alteration in the decrease in IOP seen with intramuscular cod liver oil treatment for up to 28 and 15 days respectively.
Administration, Topical↗
Modification of the fatty acid composition of rat heart sarcolemma with dietary cod liver oil, corn oil or butter.
The effect of dietary cod liver oil, corn oil or butter upon the lipid composition of cardiac sarcolemma and the activity of sarcolemmal Na+, K+ ATPase was examined in male Wistar rats. The cod liver oil diet caused significant changes in the fatty acid composition of the major phospholipids of sarcolemma, phosphatidyl choline and phosphatidyl ethanolamine. In both these phospholipids arachidonic acid, 20:4 (n - 6) was reduced by about 50% compared to rats fed butter or corn oil and was replaced by the (n - 3) fatty acids eicosapentaenoic and docosahexaenoic acids. The corn oil diet caused a significant diminution in the oleic acid content of phosphatidyl choline and elevation of linoleic acid in phosphatidyl ethanolamine. The phospholipid class composition, total phospholipid fatty acid content and cholesterol content of sarcolemma were not altered by the diets used. The activity of Na+, K+ ATPase in the cardiac sarcolemma was not significantly changed by the different diets.
Animals↗
Inhibition of atherosclerosis by cod-liver oil in a hyperlipidemic swine model.
We studied the effect of cod-liver oil on the development and progression of coronary artery disease in swine subjected to coronary balloon abrasion and fed an atherogenic diet for eight months. Sections from serial 3-mm segments of the coronary arteries were analyzed morphometrically in 7 pigs given a cod-liver-oil supplement and 11 control animals not given the supplement. Significantly less disease was seen in the sections from the animals fed cod-liver oil. The mean lesion area per vessel, mean luminal encroachment per vessel, and mean maximal luminal encroachment per vessel were reduced in animals fed cod-liver oil, as compared with controls, (P = 0.05, P = 0.016, and P = 0.011, respectively). Both groups of animals had severe hyperlipidemia throughout the study. Differences in the extent of coronary atherosclerosis were not related to differences in plasma lipid levels. Platelet arachidonate was markedly reduced, platelet eicosapentaenoic acid was increased, and serum thromboxane was decreased in the oil-fed group as compared with the control group. We conclude that in our animal mode, dietary cod-liver oil retarded the development of coronary artery disease, possibly through changes in prostaglandin metabolism.
Animals↗
Effects of dietary cod liver oil on fatty-acid composition and calcium transport in isolated adult rat ventricular myocytes and on the response of isolated hearts to ischemia and reperfusion.
Three-week-old male and female rats were placed either on standard rat chow or chow supplemented with 10% cod liver oil for 12 weeks. Animals fed cod liver oil demonstrated reduced body weights. Cod liver oil feeding produced a significant reduction in the ratio of (n - 6)/(n - 3) fatty acids in phospholipids of the isolated myocytes. The primary changes included a significant decrease in arachidonic acid (20:4, n - 6) and elevations in eicosapentaenoic acid (20:5, n - 3) and docosahexaenoic acid (22:6, n - 3). Furthermore, isolated myocytes from cod liver oil fed rats exhibited an enhanced 45Ca2+ uptake, although 45Ca2+ release was unaffected. Dietary cod liver oil had little effect on cardiac response to ischemia and reperfusion. Thus, neither developed force or resting tension was significantly affected by diet, although the latter tended to be elevated in hearts from cod liver oil fed animals. Release of creatine kinase was unaltered by diet. The release of 6-ketoprostaglandin F1 alpha from isolated hearts was significantly reduced by dietary cod liver oil, likely due to the reduced levels of arachidonic acid. Our study indicates that dietary cod liver oil and subsequent changes in phospholipid fatty-acid content are accompanied by changes in Ca2+ transport in isolated cardiac myocytes. However, this diet produces little effect on the cardiac response to acute ischemia and reperfusion.
6-Ketoprostaglandin F1 alpha↗
Dietary cod-liver oil improves endothelium-dependent responses in hypercholesterolemic and atherosclerotic porcine coronary arteries.
This study examined the effects of dietary supplementation with cod-liver oil on impaired endothelium-dependent relaxations in hypercholesterolemia and in atherosclerosis in porcine coronary arteries. Sixteen male Yorkshire pigs underwent balloon endothelium removal of the left coronary arteries and were fed a 2% high-cholesterol diet for 10 weeks, with or without dietary supplementation of cod-liver oil (30 ml/day) (oil-fed and cholesterol-fed groups, respectively). This model allowed the simultaneous examination of the effects of dietary cod-liver oil on vascular reactivity in hypercholesterolemia alone (right coronary artery) and in atherosclerosis (left coronary artery). After 10 weeks of feeding, the dietary treatment with cod-liver oil caused an increase in plasma levels of eicosapentaenoic acid and a decrease in the plasma levels of arachidonic acid, whereas the treatment had no significant effect on the increases in plasma lipid levels induced by the high-cholesterol feeding. Morphometric analysis showed significant inhibition of coronary atherosclerosis by the treatment. Endothelium-dependent responses were examined in vitro in ring preparations and in bioassay experiments. Endothelium-dependent relaxations to bradykinin, serotonin, and adenosine 5'-diphosphate were larger in both right and left coronary arteries from oil-fed than from cholesterol-fed animals. Aggregating platelets from cholesterol-fed and oil-fed pigs induced comparable, larger endothelium-dependent relaxations in rings from oil-fed than from cholesterol-fed pigs. The contractions induced by serotonin or aggregating platelets were significantly inhibited in rings with endothelium from oil-fed pigs, whereas they were comparable in rings without endothelium in both groups. Relaxations to sodium nitroprusside and contractions to potassium chloride or serotonin were comparable in rings without endothelium in both groups. The bioassay experiments revealed that the release of endothelium-derived relaxing factor in response to bradykinin and the relaxations of vascular smooth muscle to the endothelial factor were greater after the fish-oil diet. These results indicate that dietary supplementation of cod-liver oil delays the impairment of endothelium-dependent relaxations in hypercholesterolemia and in atherosclerosis, partly because of an improved release of endothelium-derived relaxing factor and partly because of an improved relaxation of coronary smooth muscle to the factor.
Animals↗
Effects of sesame and cod liver oils on prostacyclin synthesis by the rat thoracic aorta.
The influence of sesame and cod liver oils (0.5 and 1 g/kg/day s.c. for 2 weeks) on arterial PGI2 synthesis in the rat was investigated using a rat platelet antiaggregatory bioassay and HPLC methods. Smaller doses did not affect PGI2 synthesis. However, sesame oil at a dose of 1 g/kg/day significantly stimulated PGI2 synthesis, whereas cod liver oil at the same dose significantly decreased the synthesis. Incubation of control tissues in presence of exogenous arachidonic acid (33 microM) significantly stimulated PGI2 synthesis, however, incubation of cod liver oil-treated tissues in presence of arachidonic acid resulted in PGI2 synthesis, similar to that observed in the nontreated controls. The changes observed in PGI2 synthesis in the tissues from oil-treated rats may have resulted from modulation in arachidonic acid release and/or direct effects on the enzymes involved in PGI2 synthesis. The oil-induced changes in PGI2 synthesis may partly contribute towards better understanding of the biochemical mechanisms that underly some of the in vivo actions of these oils.
Animals↗
Partial normalization by dietary cod-liver oil of increased microvascular albumin leakage in patients with insulin-dependent diabetes and albuminuria.
In a double-blind crossover study, we compared the effects of eight weeks of dietary supplementation with cod-liver oil with the effects of supplementation with olive oil on endothelial permeability, blood pressure, and plasma lipid levels in 18 patients with insulin-dependent diabetes mellitus and albuminuria. When the patients received the cod-liver-oil supplement, the mean (+/- SEM) transcapillary escape rate of albumin (as compared with the base-line rate) decreased from 8.7 +/- 0.5 to 6.9 +/- 0.6 percent per hour (P less than 0.01), and the blood pressure decreased from 146 +/- 4/90 +/- 2 mm Hg to 139 +/- 4/85 +/- 2 mm Hg (P less than 0.05). There was no correlation, however, between cod-liver oil's effect on the transcapillary escape rate of albumin and its effect on blood pressure. There was no change from base line after the patients received the olive-oil supplement. During dietary supplementation with cod-liver oil, the plasma concentration of high-density lipoprotein cholesterol increased and the concentrations of very-low-density lipoprotein cholesterol and triglycerides decreased (P less than 0.05 for all comparisons), but the level of low-density lipoprotein cholesterol did not change. In contrast, during supplementation with olive oil, the concentration of low-density lipoprotein cholesterol decreased and the levels of very-low-density lipoprotein cholesterol and triglyceride increased (P less than 0.05 for all comparisons), but there was no change in the level of high-density lipoprotein. No changes were observed in the glomerular filtration rate, degree of albuminuria, insulin requirement, glycosylated hemoglobin level, or blood glucose level during supplementation with either oil. We conclude that dietary supplementation with cod-liver oil lowers the elevated transcapillary escape rate of albumin characteristic of patients with insulin-dependent diabetes and albuminuria, independently of its effect on blood pressure--perhaps by decreasing vascular permeability. We did not find any effect of cod-liver oil on urinary albumin excretion.
Adult↗
Cod liver oil does not reduce ventricular extrasystoles after myocardial infarction.
Previous work has shown that in experimental animal models a lower incidence of arrhythmias and sudden death was observed if the animals were fed cod liver oil or fish oil. After a 48-h control period starting, on average, 8 days after the onset of symptoms, 18 men who were recovering from acute myocardial infarction were given 20 ml d-1 cod liver oil for 6 weeks, either immediately after the control period, weeks 0-6 (n = 10), or during weeks 6-12 (n = 8). Forty-eight-hour Holter monitoring was carried out before cod liver oil administration and at the end of weeks 6 and 12. The eicosapentaenoic acid content of plasma phospholipids was increased by 230% during cod liver oil administration. However, no significant change was observed in the 24-h prevalence of ventricular extrasystoles or other arrhythmias during the study period. The mean ln number of ventricular extrasystoles was 2.95 +/- 0.51 (+/- SEM) during cod liver oil ingestion and 2.63 +/- 0.30 when not taking cod liver oil.
Adult↗
The effect of vitamin E (alpha-tocopherol) supplementation on hepatic levels of vitamin A and E in ethanol and cod liver oil fed rats.
Eight groups of 5 rats were fed 8 differing liquid diets with and without ethanol, cod liver oil and/or increased levels of vitamin E. Hepatic levels of vitamins A and E were determined following the 28-day feeding time. Ethanol consumption decreased the levels of hepatic vitamin E (p less than 0.05), vitamin A (p less than 0.05) and the ratio of vitamin A/E (p less than 0.05). Hepatic levels of vitamins A and E were unaffected in rats fed cod liver oil. Supplementation of the normal dietary level of 30 IU of vitamin E per kg diet, with an additional 142 IU alpha tocopherol/kg diet, restored hepatic concentrations of vitamin E to normal levels in alcohol-fed rats. The hepatic levels of vitamin A in rats fed ethanol diets supplemented with vitamin E were less than that of control rats but were 4.3 times greater than that of rats on ethanol diets unsupplemented with vitamin E. However, the vitamin A and E ratio was equal to normal in this group of rats. The vitamin A/E ratio was reduced in liver of rats fed non-alcoholic diets supplemented with vitamin E due to increased levels of hepatic vitamin E. Additionally, rats fed cod liver oil diets containing ethanol also indicated decreased hepatic vitamin A and E levels. However, these levels were greater than that of rats fed only alcoholic diets suggesting that these vitamins are replaced by the vitamin A and E content in the cod liver oil.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcoholism↗