DHA

DHA/Drug Interactions:

  • AlcoholAlcohol: In human research, alcohol use by the mother increased DHA status (levels) of the newborn infant (274).
  • Anticoagulants/antiplateletsAnticoagulants/antiplatelets: In human research, DHA resulted in a decrease in collagen-induced platelet aggregation and thromboxane A2 levels (147). However, this is not always the case. In human research, DHA had a lack of an effect on blood coagulation, platelet function, or thrombotic tendencies in healthy males (148). In human research, the antithrombotic and vasodilating agent cilostazol increased plasma DHA levels (275). In clinical research, DHA supplementation increased the activity of plasminogen activator inhibitor type 1 (PAI-1) (a component of the coagulation system that downregulates fibrinolysis in circulation) (146). According to reviews, aspirin triggered the development of DHA-derived resolvins (metabolites of DHA) and docosatrienes (metabolites of DHA) (276; 277; 278; 279). According to a review, aspirin use increased tissue concentrations of DHA (280).
  • AnticonvulsantsAnticonvulsants: Epilepsy patients on carbamazepine had lower DHA status then patients not on this agent (281). The effect of certain anticonvulsants such as valproate and carbamazepine on DHA turnover in the brain of animal models has been reviewed, with the suggestion that these agents may alter phospholipase A2 activity and thus fatty acid release from brain triglycerides (282).
  • AntidiabeticsAntidiabetics: In healthy humans, DHA had a lack of an effect on fasting insulin, fructosamine, glycosylated hemoglobin, or glucose (283). However, in diabetics, DHA resulted in increased fasting glucose levels without affecting HbA1c levels (143).
  • AntihypertensivesAntihypertensives: DHA has been shown to reduce blood pressure in animal and human research (150; 122; 151; 152; 50; 124; 121; 147; 143).
  • Anti-inflammatoriesAnti-inflammatories: According to a review and in vitro research, DHA demonstrated anti-inflammatory effects (284; 285; 286; 287; 288). However, the results were not consistent. In humans, it had a lack of an anti-inflammatory effect (289; 290; 291; 292; 293). According to reviews, supplementation with fatty acids such as DHA might reduce the increased risk of myocardial infarction and stroke attributed to use of selective COX-2 inhibitors and might have additive effects with these inhibitors for cancer and the prevention of thrombotic events (294; 295).
  • AntilipemicsAntilipemics: In humans, DHA has modified lipid levels (8; 5; 6; 7; 1; 133; 134; 135; 4; 3; 136; 137; 138; 139; 2; 140; 141; 121; 142; 143). In clinical research, high DHA fish oil resulted in triglyceride and cholesterol reductions and increased cholesterol reduction over statin use alone (144); however, simvastatin had a lack of an effect on DHA levels in blood but did increase the ratio of arachidonic acid to DHA (145).
  • AntineoplasticsAntineoplastics: According to a review, DHA may be used as a marker for the modification of cisplatin resistance (296). DHA-paclitaxel (Taxoprexin?) is a chemotherapy agent based on the ability of DHA to be taken up by cancer cells, thus increasing the bioavailability of paclitaxel. This agent has been studied in various phase II and dose toxicity studies (297; 298; 299; 300; 301). In epidemiological research, increased erythrocyte phosphatidylcholine DHA was associated with decreased prostate cancer risk (45). Apoptosis of cancer cells has been shown in in vitro research (302; 303; 304). In vitro, DHA altered the expression of target proteins of cancer therapy in chemotherapy-resistant cells (305).
  • Folic acidFolic acid: According to a review, folic acid supplementation improved plasma concentrations of DHA (306). In human research, red blood cell folate levels were correlated with plasma DHA (307).
  • Heart rate-regulating agentsHeart rate-regulating agents: According to animal research, DHA may alter heart rate and blood pressure by incorporating into cardiac phospholipids and altering heart function (151; 152; 50; 120; 124; 4; 122).
  • Hormonal agentsHormonal agents: Use of hormone replacement therapy by postmenopausal women resulted in a decrease in retroconversion of DHA to EPA (4) and an increase in blood levels of DHA and EPA (308). In women on oral contraceptives, DHA concentrations were higher than women not using oral contraceptives (309). Hormonal therapies in women, such as raloxifene and conjugated equine estrogens plus medroxyprogesterone acetate increased DHA status in blood (310).
  • ImmunosuppressantsImmunosuppressants: In human research, supplementation with DHA-rich fish oil or algal oil resulted in modifications in lymphocyte count and activation, as well as cytokine secretion and activity (153; 154; 155; 156; 157; 158; 311).
  • Iron saltsIron salts: In iron-deficient patients, iron and vitamin C supplementation resulted in increased DHA status in plasma and red blood cells (312).
  • Mood stabilizersMood stabilizers: The effect of antimanic drugs (lithium, valproate, and carbamazepine) on DHA turnover in the brain of animal models has been reviewed by Chen, with the suggestion that these agents may alter phospholipase A2 activity and thus fatty acid release from brain triglycerides (282).
  • Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonistsPeroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists: Oxidized DHA metabolites have been identified as a ligand for PPAR-gamma (313). In clinical research, DHA supplementation increased activity of plasminogen activator inhibitor type 1 (PAI-1) (146).
  • TobaccoTobacco: In human research, alcohol and tobacco use by the mother increased the DHA status of the newborn infant (274).
  • VasodilatorsVasodilators: In human research, the antithrombotic and vasodilating agent cilostazol increased plasma DHA levels (275). DHA enhanced vasodilator mechanisms and attenuated constrictor responses, perhaps due to improvements in endothelium-independent mechanisms (314).

    • DHA/Herb/Supplement Interactions:

  • Alpha-linolenic acidAlpha-linolenic acid: According to human research, consuming diets rich in alpha-linolenic acid may decrease conversion into long-chain omega-3 fatty acids, such as EPA and DHA (315). Not all studies have found this; however, the majority of studies investigating the effect of alpha-linolenic acid increases in the diet have not found an increase in blood DHA status in healthy adults (316; 317).
  • Anticoagulants/antiplateletsAnticoagulants/antiplatelets: In human research, DHA resulted in a decrease in collagen-induced platelet aggregation and thromboxane A2 levels (147). However, this was not always the case. In human research, DHA had a lack of an effect on blood coagulation, platelet function, or thrombotic tendencies in healthy males (148). In clinical research, DHA supplementation increased activity of plasminogen activator inhibitor type 1 (PAI-1) (a component of the coagulation system that downregulates fibrinolysis in circulation) (146).
  • AnticonvulsantsAnticonvulsants: Epilepsy patients on carbamazepine had a lower DHA status (significance unknown) than patients not on this agent (281). The effect of certain anticonvulsants on DHA turnover in the brain of animal models; these agents may alter phospholipase A2 activity and thus fatty acid release from brain triglycerides (282).
  • Anti-inflammatoriesAnti-inflammatories: According to a review and in vitro research, DHA demonstrated anti-inflammatory effects (284; 285; 286; 287; 288). However, the results were not consistent. In humans, it had a lack of an anti-inflammatory effect (289; 290; 291; 292; 293). According to reviews, supplementation with fatty acids such as DHA might reduce the increased risk of myocardial infarction and stroke attributed to use of selective COX-2 inhibitors and might have additive effects with these inhibitors for cancer and the prevention of thrombotic events (294; 295).
  • AntilipemicsAntilipemics: In humans, DHA has modified lipid levels (8; 5; 6; 7; 1; 133; 134; 135; 4; 3; 136; 137; 138; 139; 2; 140; 141; 121; 142; 143).
  • AntineoplasticsAntineoplastics: In epidemiological research, increased erythrocyte phosphatidylcholine DHA was associated with decreased prostate cancer risk (45). Apoptosis of cancer cells has been shown in in vitro research (302; 303; 304). According to a review, an increased response to chemopreventive agents in patients using DHA was recognized (318).
  • Arachidonic acidArachidonic acid: In adults with mild cognitive dysfunction, a combination of AA and DHA increased immediate memory and attention scores (319), and in elderly individuals, DHA and AA supplementation increased coronary flow velocity during hyperemia (320). Supplementation of infant formula with AA and DHA reduced the incidence of bronchiolitis (257), altered antigen expression on T cells (155), reduced the incidence of necrotizing enterocolitis (NEC) (258), had a lack of an effect on growth (259; 260; 261; 262; 263; 321), reduced heart rate (322), increased lean body mass and decreased fat mass (260), and improved neurodevelopment response, developmental quotient, and visual acuity in most, but not all, studies (264; 265; 15; 261; 266; 267; 268; 269; 270; 263; 323; 324). Neurodevelopment benefits lasted up to four years of age (271).
  • Cardiovascular agentsCardiovascular agents: According to animal research, DHA may alter heart rate and blood pressure by incorporating into cardiac phospholipids and altering heart function (151; 152; 50; 120; 124; 4; 122; 124; 147; 143; 122).
  • CarnitineCarnitine: In vegetarians, carnitine supplementation had a lack of an effect on DHA status in red blood cells or plasma (325).
  • Cod liver oilCod liver oil: Cod liver oil, although not a common fish body oil supplement due to its high vitamin A levels, did increase DHA in human plasma lipids (326).
  • Conjugated linoleic acid (CLA)Conjugated linoleic acid (CLA): In human research, CLA had a lack of an effect on DHA status, suggesting that it did not increase synthesis of DHA from alpha-linolenic acid (327).
  • CopperCopper: In human research, copper depletion resulted in an increase in DHA in serum phospholipids (328).
  • Echium oilEchium oil: The oil of Echium, a plant containing the omega-3 fatty acid stearidonic acid, did not increase DHA status, in human research (329).
  • EPAEPA: In human research, supplementation with EPA in the absence of DHA resulted in a decline in DHA concentration in red blood cells (330).
  • Essential fatty acids (EFAs)Essential fatty acids (EFAs): In hyperphenylalaninemic children supplemented with a combination of gamma-linolenic acid (omega-6), AA, EPA, and DHA demonstrated improved DHA status (66).
  • Evening primrose oilEvening primrose oil: Evening primrose oil, high in the omega-6 fatty acid gamma-linolenic acid, did not result in a decrease in plasma DHA in patients with skin problems undergoing hemodialysis (331).
  • FolateFolate: According to a review, folic acid supplementation improved plasma concentrations of DHA (306). In human research, red blood cell folate levels were positively correlated with plasma DHA (307).
  • Gamma-linolenic acidGamma-linolenic acid: The addition of gamma-linolenic acid (GLA; omega-6) to DHA-enriched formula for infants had a lack of an effect on DHA levels but prevented the decline in AA commonly seen following use of formula enriched with DHA in the absence of AA (332). In hyperphenylalaninemic children supplemented with a combination of gamma-linolenic acid (omega-6), AA, EPA, and DHA demonstrated improved DHA status (66).
  • Hormonal agentsHormonal agents: Use of hormone replacement therapy by postmenopausal women resulted in a decrease in retroconversion of DHA to EPA (4) and an increase n blood levels of DHA and EPA (308). In women on oral contraceptives, DHA concentrations were 10% higher than in women not using oral contraceptives (309). Hormonal therapies in women, such as raloxifene and conjugated equine estrogens plus medroxyprogesterone acetate, increased DHA status in blood (310).
  • HypoglycemicsHypoglycemics: In healthy humans, DHA had a lack of an effect on fasting insulin, fructosamine, glycosylated hemoglobin, or glucose (283). However, in diabetics, DHA resulted in increased fasting glucose levels without affecting HbA1c levels (143).
  • HypotensivesHypotensives: DHA has been shown to reduce blood pressure in animal and human research (150; 151; 152; 50; 124; 121; 124; 147; 143; 122).
  • ImmunomodulatorsImmunomodulators: In human research, supplementation with DHA-rich fish oil or algal oil resulted in modifications in lymphocyte count and activation, as well as cytokine secretion and activity (153; 154; 155; 156; 157; 158; 311).
  • IronIron: In iron-deficient patients, iron and vitamin C supplementation resulted in increased DHA status in plasma and red blood cells (312).
  • LuteinLutein: In human research, a combination of lutein plus DHA resulted in greater differences in lipoproteins when compared to lutein or DHA alone (164). Although some retinal degeneration patients in a lutein study were also taking DHA, the combined effects of these two supplements over lutein or DHA alone were not discussed (333).
  • Mood stabilizersMood stabilizers: The effect of antimanic agents on DHA turnover in the brain of animal models has been reviewed by Chen, with the suggestion that these agents may alter phospholipase A2 activity and thus fatty acid release from brain triglycerides (282).
  • Myristic acidMyristic acid: Myristic acid, an atherogenic saturated fatty acid, resulted in increased levels of DHA in plasma phospholipids (334).
  • Seal oilSeal oil: In human research, seal oil supplementation resulted in increased DHA in serum and nonesterified fatty acid fractions (335).
  • Stearidonic acidStearidonic acid: Stearidonic acid, a land-based source of omega-3 fatty acids, did not increase plasma or red blood cell DHA status in human research (336).
  • VasodilatorsVasodilators: In human research, an antithrombotic and vasodilating agent increased plasma DHA levels (275). DHA enhanced vasodilator mechanisms and attenuated constrictor responses, perhaps due to improvements in endothelium-independent mechanisms (314).
  • Vitamin AVitamin A: In retinitis pigmentosa patients also on vitamin A for four years, DHA slowed down the course of the disease after two years, but not four years (174; 337).
  • Vitamin CVitamin C: In iron-deficient patients, iron and vitamin C supplementation resulted in increased DHA status in plasma and red blood cells (312).
  • Vitamin EVitamin E: In human research, DHA supplementation for four years resulted in a trend toward lower vitamin E concentrations (338). In human research on hemodialysis patients, a combination of gamma-tocopherol and DHA resulted in significant decreases in interleukin-6 and white blood cell count (339). The clinical significance of this is not clear.
  • ZincZinc: In vitro (human neuronal cells), zinc and DHA had opposing effects on the expression levels of histones H3 and H4 (340).

    • DHA/Food Interactions:

  • Cholesterol infant formulaCholesterol infant formula: Cholesterol fortification of infant formula resulted in improved DHA status of red blood cell membranes in infants (341).
  • Cod liver oilCod liver oil: Cod liver oil, although not a common fish oil supplement due to its high vitamin A levels, did increase DHA in human plasma lipids (326).
  • CopperCopper: In human research, dietary copper depletion resulted in an increase in DHA in serum phospholipids (328).
  • Dietary alpha-linolenic acidDietary alpha-linolenic acid: According to human research, consuming diets rich in alpha linolenic acid may decrease conversion into long-chain omega-3 fatty acids, such as EPA and DHA (315). Not all studies have found this; however, the majority of studies investigating the effect of alpha-linolenic acid increases in the diet have not found an increase in blood DHA status in healthy adults (316; 317; 342; 343).
  • Dietary carnitineDietary carnitine: In vegetarians, carnitine supplementation had a lack of an effect on DHA status in red blood cells or plasma (325).
  • Dietary EPADietary EPA: In human research, supplementation with EPA in the absence of DHA resulted in a decline in DHA concentration in red blood cells (330).
  • Dietary fatty acidsDietary fatty acids: In hyperphenylalaninemic children supplemented with gamma-linolenic acid (omega-6), AA, EPA, and DHA improved DHA status (66).
  • Dietary folateDietary folate: According to a review, folic acid supplementation improved plasma concentrations of DHA (306). In human research, red blood cell folate levels were positively correlated with plasma DHA (307).
  • Dietary gamma-linolenic acidDietary gamma-linolenic acid: The addition of gamma-linolenic acid (omega-6) to DHA-enriched formula for infants had a lack of an effect on DHA levels but prevented the decline in AA commonly seen following use of formula enriched with DHA in the absence of AA (332).
  • Dietary ironDietary iron: In iron-deficient patients, iron and vitamin C supplementation resulted in increased DHA status in plasma and red blood cells (312).
  • Dietary linoleic acidDietary linoleic acid: In human research, when alpha-linolenic acid levels were maintained, increasing linoleic acid (omega-6) in the diet had a lack of an effect on DHA levels (344).
  • Dietary luteinDietary lutein: In human research, a combination of lutein plus DHA resulted in greater differences in lipoproteins over lutein or DHA alone (164). Although some retinal degeneration patients in a lutein study were also taking DHA, the combined effects of these two supplements over lutein or DHA alone were not discussed (333).
  • Dietary myristic acidDietary myristic acid: Myristic acid, an atherogenic saturated fatty acid, resulted in increased levels of DHA in plasma phospholipids (334).
  • Dietary stearidonic acidDietary stearidonic acid: Stearidonic acid, a land-based source of omega-3 fatty acids, did not increase plasma or red blood cell DHA status in human research (336).
  • Dietary vitamin ADietary vitamin A: In retinitis pigmentosa patients also on vitamin A, DHA slowed down the course of disease after two years, but not four years (174; 337).
  • Dietary vitamin CDietary vitamin C: In iron-deficient patients, iron and vitamin C supplementation resulted in increased DHA status in plasma and red blood cells (312).
  • Dietary vitamin EDietary vitamin E: In human research, DHA supplementation for four years resulted in a trend towards lower vitamin E concentrations (338). In human research on hemodialysis patients, a combination of gamma-tocopherol and DHA resulted in significant decreases in interleukin-6 and white blood cell count (339).
  • Eggs (DHA-enriched)Eggs (DHA-enriched): DHA-enriched eggs resulted in increased DHA status in human research, as well as benefits on triglyceride levels (345; 225; 346; 347; 348).
  • Evening primrose oilEvening primrose oil: Evening primrose oil, high in the omega-6 fatty acid gamma-linolenic acid, did not result in a decrease in plasma DHA in patients with skin problems undergoing hemodialysis (331).
  • FishFish: In Tanzania, serum DHA levels were 5.93% in high fish eaters vs. 1.49% in people on a mainly vegetarian diet (349).
  • Flaxseed and flaxseed oilFlaxseed and flaxseed oil: Flax or flaxseed oil, excellent sources of alpha-linolenic acid, had a lack of an effect on breast milk, plasma, or red blood cell DHA levels in human research (350; 351; 352; 353).
  • Low-animal fat dietLow-animal fat diet: In human research, a diet low in animal fat and higher in plant-based omega-3 fatty acids resulted in increased serum DHA status (354).
  • Medium chain triglyceridesMedium chain triglycerides: Use of a high medium-chain triglyceride vs. a low medium-chain triglyceride content in infant formula resulted in decreased plasma DHA status in infants (355).
  • Milk (DHA-enriched)Milk (DHA-enriched): DHA-enriched milk is available on the market in North America, and its use has been reviewed (356).
  • NucleotidesNucleotides: Use of a nucleotide-enriched infant formula resulted in increased red blood cell DHA status of infants vs. formula with no added nucleotides (357).
  • Seal oilSeal oil: In human research, seal oil supplementation resulted in increased DHA in serum and nonesterified fatty acid fractions (335).
  • Total parenteral nutrition (TPN)Total parenteral nutrition (TPN): In human research, total parenteral nutrition containing fat only as a long-chain triglyceride emulsion resulted in a reduction in DHA (358). Total parenteral nutrition containing soybean oil emulsion (high alpha-linolenic acid) resulted in increased DHA status vs. safflower oil or a mix of the two oils (248). In infants, 9% alpha-linolenic acid in total parenteral nutrition did not prevent a decline in DHA levels compared with breastfed infants (202). Use of a fat emulsion in total parenteral nutrition for neonates, with added gamma-linolenic acid, resulted in a decrease in plasma DHA (359).
  • Trans-fatty acids (hydrogenated fats)Trans-fatty acids (hydrogenated fats): Levels of milk trans-fatty acids were not related to levels of milk DHA in human breast milk (360). According to a review, increased trans-fatty acid consumption may decrease action of the fatty acid desaturases, resulting in reduced formation of DHA (361).

    • DHA/Lab Interactions:

  • Albumin (urine)Albumin (urine): Dietary long-chain omega-3 fatty acids, including DHA, are inversely associated with the degree, but not with the incidence, of albuminuria in type 1 diabetes patients (362).
  • Blood glucose and HbA1cBlood glucose and HbA1c: In diabetics, DHA resulted in increased fasting glucose levels without affecting HbA1c levels (143). In humans, DHA improved the insulin sensitivity index (178).
  • Blood pressureBlood pressure: DHA has been shown to reduce blood pressure in animal and human research (150; 122; 124; 121). According to animal research, DHA may alter heart rate and blood pressure by incorporating into cardiac phospholipids and altering heart function (151; 152; 50).
  • Coagulation panelCoagulation panel: In human research, DHA resulted in a decrease in collagen-induced platelet aggregation and thromboxane A2 levels (147). In clinical research, DHA supplementation increased activity of plasminogen activator inhibitor type 1 (PAI-1) (a component of the coagulation system that downregulates fibrinolysis in circulation) (146).
  • DHA blood status (other lipids)DHA blood status (other lipids): In human research, fish oil supplementation resulted in a preferential DHA incorporation in postprandial very-low-density lipoprotein triglycerides, and DHA supplementation resulted in increased DHA in triglycerides (363; 364). In infants, a formula enriched with DHA resulted in increased DHA in HDL and LDL phospholipid fractions (365). In adults, DHA increased DHA levels in nonesterified fatty acids (366). Most studies do not support an increase of DHA in cholesteryl esters following supplementation with DHA (367).
  • DHA blood status (phospholipid)DHA blood status (phospholipid): Algal DHA has been shown to increase plasma, platelet, neutrophil, and red blood cell DHA status in infants, children, and adults, and it was dose dependent (368; 369; 370; 124; 5; 10; 252; 207; 149; 371; 221; 209; 372; 373; 262; 374; 375; 376; 377; 338; 378; 128; 173; 127; 332; 366; 367; 379; 380; 15; 381). Phosphatidylcholine and phosphatidylethanolamine are two such phospholipids that gain DHA. Plasma phospholipid DHA status increased within 3-6 weeks of supplementation (366; 368), whereas red blood cell phospholipids took longer.
  • EPA (based on retroconversion)EPA (based on retroconversion): In human research, supplementation of DHA results in increases in phospholipid levels of EPA in plasma and platelets, suggesting retroconversion of DHA to EPA (5; 382; 4; 383; 376; 384; 367).
  • EstrogensEstrogens: In human research, DHA had a lack of an effect on estrogen metabolism with respect to the ratio of urinary 2-hydroxyestrone (2-OHE(1)) to 16alpha-hydroxyestrone (16alpha-OHE(1)) (3).
  • Fatty acid transport proteinsFatty acid transport proteins: In human research, DHA supplementation of pregnant women resulted in a correlation of mRNA expression of fatty acid transport proteins (FATP-1 and FATP-4) (385).
  • Fatty acidsFatty acids: In human research, supplementation with DHA resulted in a decrease in various cellular and plasma phospholipids, including AA, 22:4n-6, and 22:5n-6 (386).
  • Heart rateHeart rate: In human research, DHA supplementation resulted in reduced heart rate (124; 120; 4; 122). According to animal research, DHA may alter heart rate by incorporating into cardiac phospholipids and altering heart function (151; 152; 50). In human research, DHA-rich fish oil lowered heart rate during submaximal exercise (160). DHA-rich fish oil also increased heart rate variability in overweight or obese adults (161).
  • HomocysteineHomocysteine: Following supplementation with marine omega-3 fatty acids, serum phospholipid DHA status was inversely correlated with plasma homocysteine levels (387).
  • Immune function testsImmune function tests: In human research, DHA-rich oil resulted in decreased T lymphocyte activation (as assessed by expression of CD69) (153); decreases in interleukin-6 (IL-6), IL-1beta, and granulocyte colony-stimulating factor secretion after stimulation of PBMCs with lipopolysaccharide (154); fewer CD8+ mononuclear cells expressing CD25 and CD80, and lower proportions of CD14+ cells with a higher proportion of CD54+ cells upon mitogen stimulation (155). In human research, supplementation with DHA-rich fish oil resulted in increased phagocytic activity in neutrophils and monocytes, as well as neutrophil chemotactic response, production of reactive oxygen species, and increased secretion of IL-10, interferon-gamma, and tumor necrosis factor-alpha (157). In human research, DHA supplementation resulted in a reduction in endothelial expression of vascular cell adhesion molecule 1 (VCAM-1), E-selectin, intercellular adhesion molecule-1 (ICAM-1), interleukin 6 (IL-6), and IL-8 in response to IL-1, IL-4, tumor necrosis factor, or bacterial endotoxin; it also reduced the adhesion of human monocytes and monocytic U937 cells to cytokine-stimulated endothelial cells (158).
  • Inflammatory markersInflammatory markers: In humans, DHA resulted in a significant decrease in the number of circulating neutrophils, C-reactive protein (15%), and granulocyte monocyte-colony stimulating factor (123). The anti-inflammatory matrix metalloproteinase-2 was significantly increased (7%) (all p<0.05). It was suggested that DHA may lessen the inflammatory response by altering the fatty acid composition of blood lipids. In humans, it was also noted that DHA resulted in increased plasma IL-10 vs. placebo (p=0.021) (134).
  • Lipid profileLipid profile: DHA has been shown to reduce triglyceride and increase HDL cholesterol levels in human research (1; 388; 4; 8; 133; 6; 5; 135; 138). According to human research, DHA supplementation may increase levels of total and LDL cholesterol in normolipidemic and hyperlipidemic individuals (7; 3; 136; 137; 139; 2; 140; 133; 138). In other human research, DHA supplementation resulted in a reduction in total cholesterol, LDL cholesterol, and apolipoprotein B levels (3; 140; 389). DHA supplementation resulted in increases in large LDL and large HDL particle concentrations and decreased concentrations of small LDL and medium HDL particles in human research (134).
  • LDL oxidationLDL oxidation: In human research, although EPA supplementation resulted in increased formation of conjugated dienes during LDL oxidation; DHA supplementation did not (390). In human research, DHA supplementation resulted in increased ex vivo oxidative susceptibility of LDL and increased conjugated dienes (391).
  • NorepinephrineNorepinephrine: Results from human research suggest that the antistress effects of DHA may be associated with significant reductions in norepinephrine, with increased ratios of epinephrine to norepinephrine (392; 393).
  • Phospholipid levelsPhospholipid levels: In human research, supplementation of DHA resulted in increases in phospholipid levels of EPA in plasma and platelets, suggesting retroconversion of DHA to EPA (5; 382; 4; 383; 376; 384; 367).
  • Red blood cell omega-3 indexRed blood cell omega-3 index: In human research, DHA supplementation resulted in a beneficial increase in the red blood cell omega-3 index, a risk factor for cardiovascular disease (383).
  • Serum proteinSerum protein: Total serum protein was elevated in the DHA-enriched egg treatment group (10.3% vs. 1.3% for ordinary eggs; p=0.034) of a human study (133).
  • Urinary F2-isoprostanesUrinary F2-isoprostanes: In human research, DHA supplementation resulted in a reduction in urinary F2 isoprostanes (193; 394).
  • Vitamin E levelsVitamin E levels: In human research, DHA supplementation for four years resulted in a trend toward lower vitamin E concentrations (338). In human research, DHA supplementation resulted in a decrease in tocopherol in LDL (391).