Stroke and plasma markers of milk fat intake – a prospective nested case-control study

Background  

Dairy products are high in saturated fat and are traditionally a risk factor for vascular diseases. The fatty acids 15:0 and 17:0 of plasma lipids are biomarkers of milk fat intake. The aim of the present study was to evaluate the risk of a first-ever stroke in relation to the plasma milk fat biomarkers.     

Dietary intake of fish vs. formulations leads to higher plasma concentrations of n−3 fatty acids

The n−3 fatty acids from fish appear to be more efficacious, in terms of cardioprotection, than equivalent amounts provided as capsules. Volunteers were given, for 6 wk, either 100 g/d of salmon, providing 383 mg of EPA and 544 mg of DHA, esterified in glycerol lipids, or 1 or 3 capsules of fish oil/d, providing 150 mg of EPA and 106 mg of DHA or 450 mg of EPA and 318 mg of DHA, as ethyl esters. Further, we reevaluated data from a previous study carried out with the same design, i.e., with 3 and 6 capsules/d of fish oil, providing 1290 and 2580 mg/d EPA and 960 and 1920 mg/d DHA. Marked increments in plasma EPA and DHA concentrations (μg/mg total lipid) and percentages of total fatty acids were recorded at the end of treatment with either n−3 capsules or salmon. Net increments of EPA and DHA in plasma lipids were linearly and significantly correlated with the dose after capsule administration. Further, increments in plasma EPA and DHA concentration after salmon intake were significantly higher than after administration of capsules. The same increments would be obtained with at least two- and ninefold higher doses of EPA and DHA, respectively, if administered with capsules rather than salmon. We provide experimental evidence that n−3 fatty acids from fish are more effectively incorporated into plasma lipids than when administered as capsules and that increments in plasma concentrations of EPA and DHA given as capsules are linearly correlated with their intakes.     

Should the forms of dietary choline also be considered when estimating dietary intake and the implications for health?

Although epidemiological studies suggest that populations are not meeting daily recommendations for total choline, they fail to consider the forms of choline in the diet. Aqueous and lipid‐soluble choline forms differ in absorption, metabolism and functions, suggesting that the form matters. It has been demonstrated that the relative amount of these forms of choline can be altered through consuming different foods and using different preparation methods. Evidence suggests that the forms of choline may differentially impact growth, immune function, plasma and serum cholesterol levels and brain development, therefore in addition to estimating the amount total choline in the diet, researchers should also consider what forms of choline are consumed in the diet.     

Is the relatively low intake of omega‐3 fatty acids in Western diet contributing to the obesity epidemics?

Alongside the increase of overweight and obesity in the world there is the avoidance of saturated fat and an increased dietary use of vegetable oils rich in omega‐6 fatty acids. These changes result in a marked increase of the omega‐6/omega‐3 ratio and there is increasing evidence that this changed balance is related to lifestyle diseases. There are also indications that this balance between fatty acids may be involved in epigenetics, i. e. that it influences metabolic pathways during intra‐uterine or early life which cause diseases later in life. Such processes would be a possible explanation for the epidemic outburst of obesity during the latest decades.     

The tocopherol pattern in human serum is markedly influenced by intake of vitamin E drugs—Results of the german national health surveys

During national and regional health surveys, done from 1984–1995 in Germany, consumption data for all drugs used by the participants—approximately 18,000 persons—in the last 7 d before the examination were monitored with a detailed drug-usage questionnaire. The groups examined are representative for the national and regional German inhabitant population aged 25–69 yr. In serum samples of subsamples of the study participants, all tocopherols were measured by isocratic high-performance liquid chromatography (Si 60 column, fluorescence detection). Consumption data for tocopherol-containing drugs showed that up to 5% of females and up to 3% of males of the study population used those drugs. During the study period, the serum content of α-tocopherol (mean values ± SD) rose from 7.5 ± 2.6 mg/L serum to 11.8 ± 2.8 mg/L serum for nonusers and from 11.9 ± 4.3 mg/L serum to 15.3 ± 4.9 mg/L serum in tocopherol-drug users. Throughout all studies, it could be shown that β- and γ-tocopherol were heavily reduced in those persons taking daily doses ≥50 mg α-tocopherol. The reduction of the two tocopherols is dose-dependent and especially pronounced in females using high-dose α-tocopherol drugs. Owing to the emerging evidence of the physiological importance concerning the balance of the different tocopherols in biological systems, the possible benefits of using natural tocopherol mixtures from plant origin instead of pure RRR-α-tocopherol, gained from permethylation procedures, as vitamin supplements in human nutrition should be considered.     

Increased α-linolenic acid intake increases tissue α-linolenic acid content and apparent oxidation with little effect on tissue docosahexaenoic acid in the guinea pig

The essential fatty acids do not have identical roles in nutrition. Linoleic acid (LA) accumulates throughout the body of most mammals, whereas α-linolenic acid (ALA) is rarely found in tissue lipids to the same extent as LA. It has been argued that this is the result of metabolism of ALA to docosahexaenoic acid (DHA) or that ALA is rapidly β-oxidized to acetyl CoA and CO₂. In this study, we consider the effect of high and low ALA levels on the tissue distribution of ALA and other n-3 polyunsaturated fatty acids (PUFA) in all tissues. Guinea pigs were fed one of two defined diets for 3 wk from wearning with both diets containing 1.8% (by weight) of LA and either 1.7% ALA or 0.03% ALA. The high ALA diet was associated with significantly increased ALA levels in all tissues except the brain and significantly increased levels of long-chain n-3 PUFA in all tissues except intestines, brain, carcass, and skin. The long-chain n-3 PUFA content of the whole body was less than 5% of that of the ALA content in both diet groups, and the major long-chain n-3 PUFA (>66% of total) in the body was 22∶5n−3. The brain was the only tissue where the DHA content exceeded that of 22∶5n−3. On the low ALA diet, there appeared to be conservation of ALA based on a comparison of the ratio of LA to ALA in the tissues compared with that in the diet. On the high ALA diet there was a loss of ALA relative to LA in the tissues compared with the diet. These studies suggest that the low levels of tissue ALA in the guinea pig are likely the result of β-oxidation or excretion via the skin and fur rather than metabolism to DHA.     

Markedly raised intake of saturated and monounsaturated fatty acids in rats on a high-fat ketogenic diet does not inhibit carbon recycling of13C-α-linolenate

Under various dietary and physiological conditions, carbon from α-linolenic acid (ALA) is extensively recycled into saturated and monounsaturated fatty acids. In this study we investigated whether carbon is still recycled from ALA when a dietary source of saturated and monounsaturated fatty acids is provided in excess.¹³C-labeled ALA was given to rats consuming a high-fat ketogenic diet and to rats consuming a low-fat control diet. In rats on the ketogenic diet,¹³C recycling from α-linolenate into several, but not all, saturated and monounsaturated fatty acids matched or exceeded that in the controls (P<0.05). We conclude that carbon recycling into saturated and monounsaturated fatty acids persists when the main end products of ALA recycling are provided in excess, using a ketogenic diet.