BackgroundBeneficial effects of omega-3 polyunsaturated fatty acids (n-3 PUFAs) on the lipid levels of dyslipidemic subjects are widely described in the literature. However, the underlying molecular mechanisms are largely unknown. The aim of this study was to investigate the effects of n-3 PUFAs on the expression of lipid metabolism-related genes in normo- and dyslipidemic men to unveil potential genes and pathways affecting lipid metabolism.MethodsTen normo- and ten dyslipidemic men were supplemented for twelve weeks with six fish oil capsules per day, providing 1.14 g docosahexaenoic acid and 1.56 g eicosapentaenoic acid. The gene expression levels were determined by whole genome microarray analysis and quantitative real-time polymerase chain reaction.ResultsSeveral transcription factors (peroxisome proliferator-activated receptor α (PPARα), retinoid X receptor (RXR) α, RXRγ, hepatic nuclear factor (HNF) 6, and HNF1ß) as well as other genes related to triacylglycerol (TG) synthesis or high-density lipoprotein (HDL-C) and cholesterol metabolism (phospholipids transfer protein, ATP-binding cassette sub-family G member 5, 2-acylglycerol O-acyltransferase (MOGAT) 3, MOGAT2, diacylglycerol O-acyltransferase 1, sterol O-acyltransferase 1, apolipoprotein CII, and low-density lipoprotein receptor) were regulated after n-3 PUFA supplementation, especially in dyslipidemic men.ConclusionGene expression analyses revealed several possible molecular pathways by which n-3 PUFAs lower the TG level and increase the HDL-C and low-density lipoprotein level, whereupon the regulation of PPARα appear to play a central role.Trial registrationClinicalTrials.gov (ID: NCT01089231)

Introduction: Studies indicate that 17.9% -60% of adults in Germany and Europe regularly use food supplements. Some reports suggest that their use might be responsible for excessive nutrient intake. The purpose of this survey was to examine the quantitative mineral intakes from food supplements: whether the tolerable upper intake levels (ULs) with supplements alone, or in combination with food was exceeded was checked. Methods: The survey was carried out by the Association for Consumer Research, Nürnberg, Germany. Anonymous data of 1070 supplement users (40.8% men, 59.2% women) aged 18 -93 years were available. Three groups were examined based on dietary and supplemental mineral intakes: average, middle-high and high intake. Results: The mean number of supplements reported was 1.6 ± 1.1 products in men and 1.5 ± 0.9 products in women. The minerals most frequently consumed were magnesium, followed by calcium, zinc and selenium. The percentage of the supplement users with total intakes greater than the UL was minimal for all minerals. Supplement use in 143 cases increased the likelihood of intakes above the UL only for magnesium. Subjects particularly in the high intake group-as a worst case scenario-had intakes above the UL in the case of calcium (n = 23) and zinc (n = 34). The percentage of subjects taking several products was greater in subjects exceeding the UL than in those below (P < 0.001). Multiple use was seen significantly more often in men than in women (P < 0.01). Conclusions: In this survey, supplement use was generally not associated with excessive intake. Supplement use resulted in intakes above the UL in only a few cases relating to magnesium, calcium and zinc. This applies more often to elderly subjects and particularly to those who already have a high mineral intake from food in the model calculation.

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These findings indicate an association between several FADS genotypes for higher n-6 and n-3 precursor PUFA and lower AA levels in erythrocyte membranes in minor compared to major allele carriers. To what extent FADS genotypes and a lower conversion of LA and ALA to biologically important LC PUFAs such as AA, EPA and DHA contributes to cognitive decline should be investigated in further trials. Nevertheless, the omega-3 index in this cohort of MCI patients can be classified as insufficient.

Food supplements, if not properly used, may lead to potentially harmful nutrient intake. The purpose of this survey was to examine vitamin intake from food supplements. Taking into account the intake from food, as obtained from the National Nutrition Survey, it was determined whether the tolerable upper intake levels (ULs) were exceeded via supplements alone, or in combination with food. Data from 1070 supplement users (18-93 years) was available. The dietary and supplemental vitamin intakes of three groups were analyzed: average intake (50th percentile food+50th percentile supplements), middle-high intake (50th+95th) and high intake (95th+95th). Vitamin C (53%), vitamin E (45%) and B vitamins (37-45%) were consumed most frequently. Few subjects (n=7) reached or exceeded the ULs through supplements alone. The UL for vitamin A and folate was reached by a few men in the middle-high group, and by a few men and women in the high intake group. Otherwise, even in the high intake group, the recommended vitamin D intake of 20 µg/day (in case of insufficient endogenous synthesis) could not be achieved. The use of food supplements was not associated with excessive vitamin intake in this survey, except in a small number of cases. Vitamin A intake above the UL was the result of high dietary intake which also included the intake of β-carotene, rather than the result of overconsumption of food supplements. Diets mainly included folate from natural sources, which has no associated risk.

The present cross-sectional data demonstrate cardiovascular (CV) risk in patients with rheumatoid arthritis (RA). The cross-sectional data were part of an interventional trial that included 100 patients with defined RA. Traditional CV risk parameters and risk score calculation for the German population were used to assess the CV risk profile in the collective given. Proatherogenic lipid profile characterised by increased total cholesterol (≥ 5.2 mmol/l) and LDL cholesterol (≥ 3.5 mmol/l) levels was measured in 85 and 66%, respectively, of the study population. Elevated concentrations of homocysteine (≥ 10 μmol/l) were reached by 67%. The prevalence of patients at high CV risk was 12% and increased up to 42% after using a multiplication factor of 1.5. No association was seen between the CV risk SCORE and DAS 28 or disease duration. RA patients in this study showed a proatherogenic risk profile with regard to the CV risk factors evaluated. The calculation of a 10-year risk using German risk charts might have led to an overall underestimation of the mean CV risk. Cardiovascular co-morbidity in RA patients must be seen as a major prevention and treatment target and should be monitored adequately.

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Elevated circulating concentrations of total L-homocysteine (thCys) and free asymmetric dimethylarginine (ADMA) are long-established cardiovascular risk factors. Low circulating L-homoarginine (hArg) concentrations were recently found to be associated with increased cardiovascular morbidity and mortality. The biochemical pathways of these amino acids overlap and share the same cofactor S-adenosylmethionine (SAM). In the present study, we investigated potential associations between hArg, L-arginine (Arg), ADMA and thCys in plasma of patients suffering from rheumatoid arthritis (RA), coronary artery disease (CAD) or peripheral artery occlusive disease (PAOD). In RA, we did not find any correlation between ADMA or hArg and thCys at baseline (n = 100) and after (n = 83) combined add-on supplementation of omega-3 fatty acids, vitamin E, vitamin A, copper, and selenium, or placebo (soy oil). ADMA correlated with Arg at baseline (r = 0.446, P < 0.001) and after treatment (r = 0.246, P = 0.03). hArg did not correlate with ADMA, but correlated with Arg before (r = 0.240, P = 0.02) and after treatment (r = 0.233, P = 0.03). These results suggest that hArg, ADMA and Arg are biochemically familiar with each other, but unrelated to hCys in RA. In PAOD and CAD, ADMA and thCys did not correlate.