BackgroundDifferent healthy food patterns may modify cardiometabolic risk. We investigated the effects of an isocaloric healthy Nordic diet on insulin sensitivity, lipid profile, blood pressure and inflammatory markers in people with metabolic syndrome.MethodsWe conducted a randomized dietary study lasting for 18–24 weeks in individuals with features of metabolic syndrome (mean age 55 years, BMI 31.6 kg m−2, 67% women). Altogether 309 individuals were screened, 200 started the intervention after 4-week run-in period, and 96 (proportion of dropouts 7.9%) and 70 individuals (dropouts 27%) completed the study, in the Healthy diet and Control diet groups, respectively. Healthy diet included whole-grain products, berries, fruits and vegetables, rapeseed oil, three fish meals per week and low-fat dairy products. An average Nordic diet served as a Control diet. Compliance was monitored by repeated 4-day food diaries and fatty acid composition of serum phospholipids.ResultsBody weight remained stable, and no significant changes were observed in insulin sensitivity or blood pressure. Significant changes between the groups were found in non-HDL cholesterol (−0.18, mmol L−1 95% CI −0.35; −0.01, P = 0.04), LDL to HDL cholesterol (−0.15, −0.28; −0.00, P = 0.046) and apolipoprotein B to apolipoprotein A1 ratios (−0.04, −0.07; −0.00, P = 0.025) favouring the Healthy diet. IL-1 Ra increased during the Control diet (difference −84, −133; −37 ng L−1, P = 0.00053). Intakes of saturated fats (E%, beta estimate 4.28, 0.02; 8.53, P = 0.049) and magnesium (mg, −0.23, −0.41; −0.05, P = 0.012) were associated with IL-1 Ra.ConclusionsHealthy Nordic diet improved lipid profile and had a beneficial effect on low-grade inflammation.

Lipid auto-oxidation in milk is affected by a complex interplay of pro-and antioxidants. Several of these compounds are also important nutrients in the human diet and may have other physiological effects in the gastrointestinal tract and other tissues. Among antioxidative enzymes superoxide dismutase catalyses the dismutation of superoxide anion to hydrogen peroxide. The degradation of hydrogen peroxide can be catalysed by catalase and the selenoprotein glutathione peroxidase. The latter enzyme can also degrade lipid peroxides. Lactoferrin may have an important role by binding pro-oxidative iron ions. The occurrence of different forms of these antioxidative proteins in milk and available data on their functional role are reviewed. More remains to be learnt of individual compounds and as an example the potential role of seleno compounds in milk is virtually unknown. Antioxidative vitamins in milk can provide an important contribution to the daily dietary intake. Moreover vitamin E and carotenoids act as fat-soluble antioxidants, e.g. in the milk fat globule membrane, which is regarded as a major site of auto-oxidation. Vitamin C is an important water-soluble antioxidant and interacts in a complex manner with iron and fat-soluble antioxidants. The concentrations of these compounds in milk are affected by cow feeding rations and milk storage conditions. Since milk contains a number of antioxidants many reactions are possible and the specific function of each antioxidant cannot easily be defined. There are indications that other compounds may have antioxidative function and measurement of total antioxidative capacity should be a useful tool in evaluating their relative roles.

To explore the possibility that peroxtdative degradation of brain tissue lipid constituents is an important mechanism of irreversible ischemic damage, we measured cortical fatty acids and phospholipids during reversible brain ischemia in the rat. Neither complete nor severe incomplete ischemia (5 and 30 min) caused any measurable breakdown of total or individual fatty acids or phospholipids. Except for a small (and reversible) decrease of inositol plus serine phosphoglycerides in the early postischemic period following 30 min of incomplete ischemia, there were no significant losses of fatty acids or phospholipids during recirculation. Since peroxidation, induced in brain cortical tissue in vitro, characteristically involves degradation of polyenoic fatty acids (arachidonic and docosahexaenoic acids) and of ethanolamine phosphoglycerides, the present in vivo results fail to support the hypothesis that peroxidation of membrane lipids is of primary importance for ischemic brain cell damage. Both complete and severe incomplete ischemia caused a similar increase in the tissue content of free fatty acids (FFA). Thus the FFA pool increased by about 10 times during a 30‐min ischemic period, to constitute 1 ‐ 2% of the total fatty acid pool. Since there was a relatively larger increase in polyenoic FFA (especially in arachidonic acid) than in saturated FFA, the release of FFA may be the result of activation of a phospholipase A2 unbalanced by reesterification. Increased levels of FFA persisted during the initial recirculation period, but a gradual normalization occurred and the ischemic changes were essentially reversed at 30 min after restoration of circulation. The pathophysiological implications of the changes in FFA are discussed with respect to mitochondrial dysfunction, formation of cellular edema and prostaglandin‐mediated deterioration of postischemic circulation.

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