Effects of alpha-linolenic acid and quercetin on n-3 polyunsaturated fatty acid status and cardiovascular disease risk markers in metabolically healthy men and women
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Beschreibung
Epidemiological and clinical studies indicate that regular intake of omega-3 (n-3) polyunsaturated fatty acids (PUFA) may lower the risk of cardiovascular diseases (CVD) and all-cause-mortality. Most of these cardioprotective effects are attributed to the marine long-chain n-3 PUFA eicosapentaenoic acid (EPA; C20:5 n-3) and docosahexaenoic acid (DHA; C22:6 n-3). Studies about the effects of the n-3 fatty acid alpha-linolenic acid (ALA; C18:3 n-3) on CVD risk have revealed inconsistent results. Dietary ALA, which is abundant in certain plant foods, including various vegetable oils, such as linseed (flaxseed) oil and rapeseed (canola) oil, can be desaturated and elongated forming long-chain n-3 PUFA in humans. However, the extent to which this occurs, and whether ALA has physiologic effects independent of its role as a precursor for long-chain n-3 PUFA, is unclear. Data from epidemiological and animal studies suggest that the conversion of ALA to EPA and DHA may be increased through simultaneous nutritive intake of flavonoids. One of the major flavonoids in human nutrition is the flavonol quercetin (3,3',4',5,7-pentahydroxyflavone), ubiquitously distributed in edible plants, with rich sources being onions, kale, unpeeled apples, berries, citrus fruits and tea (Camellia sinensis). Quercetin is one of the most potent antioxidants of plant origin. ALA and quercetin are characteristic compounds in a plant-based cardioprotective dietary pattern. Until now, there is no clinical investigation about the (combined) effectiveness of ALA and quercetin supplementation on conversion of ALA to long-chain PUFA and on CVD risk factors in humans.
Within a randomized, single-blinded, diet-controlled crossover trial (chapter 3) the systemic availability of quercetin derived from hard capsules filled with onion skin extract powder and from hard capsules filled with pure quercetin dihydrate was determined in 12 metabolically healthy men and women. The six men and six women, aged 21 – 33 years were administered a single oral supra-nutritional dose of approximately 163 mg quercetin derived from onion skin extract powder (containing 95.3 % of total flavonoids as quercetin aglycone) or quercetin dihydrate (134 mg quercetin aglycone equivalent). Blood samples were collected before and during a 24 h period after quercetin administration. The concentrations of quercetin and its two monomethylated derivatives, isorhamnetin (3′-O-methyl quercetin) and tamarixetin (4′-O-methyl quercetin), were measured using HPLC with fluorescence detection after plasma enzymatic treatment. The plasma concentration-time curves of quercetin were 4.8 times higher and the maximum plasma concentration (Cmax) was 5.4 times higher after ingestion of the onion skin extract than after ingestion of pure quercetin dihydrate. Similiar results were shown for isorhamnetin and tamarixetin. The plasma kinetics of quercetin were not significantly different in men and women.
The second randomized, placebo-controlled, and double-blinded crossover trial (chapter 4 and chapter 5) investigated the effects of increased ALA intake (3.6 g/d) on fatty acid composition of serum phospholipids and erythrocytes in metabolically healthy men and women (n = 74) and whether fatty acid profiles and ALA conversion were affected by regular quercetin intake (190 mg/d) or gender. Both interventions significantly increased serum phospholipid ALA and EPA content, while DHA concentration showed a slight decrease. Erythrocyte ALA and EPA significantly increased with both interventions, whereas DHA decreased. Fatty acid composition did not differ between sexes and there was no effect of quercetin.
In addition, the data of the second crossover trial were investigated with regard to the potential independent and additive effects of ALA and quercetin on blood pressure (BP), lipid and glucose metabolism, as well as on biomarkers of inflammation, oxidative stress, and antioxidant status. Plasma quercetin, tamarixetin, isorhamnetin, and kaempferol increased significantly from baseline to study end under ALA and quercetin supplementation. The dietary supplements improved lipid profiles in healthy adults, while antioxidative and oxidative status, inflammation, and BP remained unchanged. No evidence was seen for an additive or synergistic effect of ALA plus quercetin on markers of cardiovascular disease risk.
In conclusion, the bioavailability of quercetin aglycone administered as hard capsules filled with natural onion skin extract powder is greater than that from capsules containing quercetin dihydrate powder and solid excipients in healthy humans. A daily supplementation with 3.6 g/d ALA over an 8-week period improved long-chain n-3 PUFA status in metabolically healthy subjects. ALA supplementation increased ALA, EPA, and DPA, but not DHA, in serum phospholipids and erythrocytes in metabolically healthy, young adults. The conversion of ALA was not affected by concomitant ingestion of a supra-nutritional dose of 190 mg/d quercetin. There were no sex-specific differences in the responses to ALA intervention. In addition, daily supplementation with 3.6 g ALA improved lipid profiles in metabolically healthy non-obese men and women. Contrary to the hypotheses, we found no evidence of an additive or synergistic effect of combined ALA plus a supra-nutritional dose of quercetin on CVD risk markers.
Autor*in
Constanze Burak