In the United States, intake of n-3 fatty acids is approximately 1.6 g/d ( approximately 0.7% of energy), of which 1.4 g is alpha-linolenic acid (ALA; 18:3) and 0.1-0.2 g is eicosapentaenoic acid (EPA; 20:5) and docosahexaenoic acid (DHA; 22:6). The primary sources of ALA are vegetable oils, principally soybean and canola. The predominant sources of EPA and DHA are fish and fish oils. Intake data indicate that the ratio of n-6 to n-3 fatty acids is approximately 9.8:1. Food disappearance data between 1985 and 1994 indicate that the ratio of n-6 to n-3 fatty acids has decreased from 12.4:1 to 10.6:1. This reflects a change in the profile of vegetable oils consumed and, in particular, an approximate 5.5-fold increase in canola oil use. The ratio of n-6 to n-3 fatty acids is still much higher than that recommended (ie, 2.3:1). Lower ratios increase endogenous conversion of ALA to EPA and DHA. Attaining the proposed recommended combined EPA and DHA intake of 0.65 g/d will require an approximately 4-fold increase in fish consumption in the United States. Alternative strategies, such as food enrichment and the use of biotechnology to manipulate the EPA and DHA as well as ALA contents of the food supply, will become increasingly important in increasing n-3 fatty acid intake in the US population.

In the present study we used regression analyses to evaluate the effects of stearic acid (18:0) on total cholesterol (TC), low-density-lipoprotein-cholesterol (LDL-C), and high-density-lipoprotein-cholesterol (HDL-C) concentrations (mmol/L). Using data from 18 articles, we developed the following predictive equations (monounsaturated fatty acids, MUFAs; polyunsaturated fatty acids, PUFAs): delta TC = 0.0522 delta 12:0-16:0 - 0.0008 delta 18:0 - 0.0124 delta MUFA - 0.0248 delta PUFA; delta LDL-C = 0.0378 delta 12:0-16:0 + 0.0018 delta 18:0 - 0.0178 delta MUFA - 0.0248 delta PUFA; delta HDL-C = 0.0160 delta 12:0-16:0 - 0.0016 delta 18:0 + 0.0101 delta MUFA + 0.0062 delta PUFA. Our analyses revealed that unlike the other long-chain saturated fatty acids (SFAs), stearic acid had no effect on TC and lipoprotein cholesterol concentrations in men and women. MUFAs elicited an independent hypocholesterolemic effect that we believe is due to the small amount of 12:0-16:0 in the experimental diets evaluated. The observation that stearic acid has unique effects on TC, LDL-C, and HDL-C provides additional compelling evidence that it be distinguished from the other major SFAs in blood cholesterol predictive equations.

1. Ageing represents a great concern in developed countries because the number of people involved and the pathologies related with it, like atherosclerosis, morbus Parkinson, Alzheimer's disease, vascular dementia, cognitive decline, diabetes and cancer. 2. Epidemiological studies suggest that a Mediterranean diet (which is rich in virgin olive oil) decreases the risk of cardiovascular disease. 3. The Mediterranean diet, rich in virgin olive oil, improves the major risk factors for cardiovascular disease, such as the lipoprotein profile, blood pressure, glucose metabolism and antithrombotic profile. Endothelial function, inflammation and oxidative stress are also positively modulated. Some of these effects are attributed to minor components of virgin olive oil. Therefore, the definition of the Mediterranean diet should include virgin olive oil. 4. Different observational studies conducted in humans have shown that the intake of monounsaturated fat may be protective against age-related cognitive decline and Alzheimer's disease. 5. Microconstituents from virgin olive oil are bioavailable in humans and have shown antioxidant properties and capacity to improve endothelial function. Furthermore they are also able to modify the haemostasis, showing antithrombotic properties. 6. In countries where the populations fulfilled a typical Mediterranean diet, such as Spain, Greece and Italy, where virgin olive oil is the principal source of fat, cancer incidence rates are lower than in northern European countries. 7. The protective effect of virgin olive oil can be most important in the first decades of life, which suggests that the dietetic benefit of virgin olive oil intake should be initiated before puberty, and maintained through life. 8. The more recent studies consistently support that the Mediterranean diet, based in virgin olive oil, is compatible with a healthier ageing and increased longevity. However, despite the significant advances of the recent years, the final proof about the specific mechanisms and contributing role of the different components of virgin olive oil to its beneficial effects requires further investigations.

The comparative absorption of cocoa butter (25.5% C16:0, 34.4% C18:0, 34.4% C18:1, 3.4% C18:2) and corn oil (11.4% C16:0, 2.0% C18:0, 26.4% C18:1, 60.0% C18:2) was assessed in six healthy male subjects. During 3-d experimental diet periods, free-living subjects consumed either cocoa butter or corn oil as virtually the sole source of dietary fat, provided at 40% of the total energy intake in the form of specially formulated cookies. Fat absorption was determined by quantifying total fecal lipid excretion over the 3-d period. Total fecal lipid and fecal fatty acids were determined. The percentage of fat excreted was significantly higher (p less than or equal to 0.001) when subjects consumed the cocoa butter (10.8 +/- 3.2%) vs the corn oil (3.5 +/- 1.0%) diet. These results indicate that the digestibility of cocoa butter is significantly less than corn oil and may explain, in part, previous reports of a neutral effect of dietary cocoa butter on plasma cholesterol concentrations.

In two experiments, young rats were preconditioned with dietary cholesterol by: 1) nursing from dams with a high cholesterol milk or, 2) receiving 10 mg cholesterol dissolved in 0.5 ml of corn oil daily from 6 to 30 days of age. When rats preconditioned with dietary cholesterol in early life were fed stock diet supplemented with 10% lard and 0.5% cholesterol ("cholesterol challenge diet") there was no protection against dietary induced hypercholesterolemia in adult life. In a third experiment, two groups of newborn rats were intubated with: 1) a cholesterol free formula, 2) the cholesterol free formula plus 50 mg% cholesterol. A third group of pups suckled normally. After weaning all pups were fed a stock diet supplemented with 10% lard and 0.5% cholesterol for 1 month. There was no difference in the serum cholesterol in either group of artificially reared rats after the "cholesterol challenge" (106 +/- 6 mg/100 ml). Suckled rats, however, had a lower serum cholesterol after the "cholesterol challenge" (75 +/- 2 mg/100 ml). All experiments conducted refute the hypothesis that early exposure to dietary cholesterol protects against dietary induced hypercholesterolemia in adult life. It appears, however, that cholesterol metabolic systems are affected in early life because of the decreased ability of artificially reared rats to handle a "cholesterol challenge." Possible factors include a component of the dam's milk, growth and development, and the psychological and emotional stress of the artificial rearing process.

Semipurified diets containing 10% kilocalories from either safflower oil (SO), corn oil (CO), olive oil (OO) or palm oil (PO) were fed to weanling male rats for 2 weeks. The effects of dietary fat saturation on plasma lipids and lipoproteins were: 1) Nonfasted plasma cholesterol concentration was higher in rats fed OO (mean +/- SEM = 81.0 +/- 2.9 mg/dl) vs. CO (67.5 +/- 2.9); 2) plasma chylomicron cholesterol concentration was higher in rats fed OO vs. SO and CO, with PO values in between; and 3) the cholesterol concentration of plasma very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL) did not differ among groups. The effects of dietary fat saturation on hepatic lipoproteins (determined by liver perfusion techniques) were: 1) hepatic higher density lipoprotein (d = 1.006-1.21 g/ml) cholesterol production was greater in rats fed SO and CO vs. PO [19.1 +/- 1.2, 17.2 +/- 0.8 and 13.7 +/- 1.6 micrograms/(g liver X 1.5 hour), respectively]; 2) there was no difference in hepatic VLDL cholesterol production among groups; and 3) the ratio of cholesterol to protein of hepatic VLDL and the higher density lipoprotein fraction was higher in rats fed diets rich in polyunsaturated fatty acids versus saturated fatty acids. Dietary fat saturation had no effect on carcass and liver cholesterol concentrations. Since differences in hepatic lipoprotein production were not reflected in plasma lipoprotein patterns, these results suggest that extrahepatic lipoprotein metabolism differs in rats fed diets containing fatty acids of varying saturation.

No abstract

Two experiments were conducted to determine the effect of dietary manganese on cholesterol and lipid metabolism in the Wistar rat and the genetically hypercholesterolemic RICO rat. Weanling animals were placed on a manganese-deficient (0.12 microgram/g) and a supplemented diet (100.12 micrograms/g). Mean body weights, hepatic fatty acid synthesis and liver manganese concentration significantly decreased in the deficient group of Wistar rats. Plasma cholesterol, VLDL (very low density lipoprotein) and HDL (high-density lipoprotein) cholesterol, hepatic cholesterol synthesis, liver cholesterol and lipid concentrations were not significantly affected by manganese deficiency. Mean body weights and hepatic manganese content were lower in the manganese-deficient group in both normal and hypercholesterolemic RICO rats. Manganese deficiency significantly decreased LDL cholesterol concentration in the hypercholesterolemic RICO rats. Manganese deficiency had no significant effect on hepatic cholesterol and fatty acid synthesis, plasma cholesterol, VLDL and HDL cholesterol concentrations, liver lipid and liver cholesterol concentration in either group of RICO rats. These results indicate that dietary manganese deficiency does not result in significant alterations in cholesterol and lipid metabolism in the rat.