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Background: The beneficial effects of n-3 polyunsaturated fatty acids (PUFA) in reducing high blood triglyceride (TG) levels have been well demonstrated. This study aimed to investigate the effect of chia seeds on blood TG and its associated cardiometabolic factors in hypertriglyceridaemic individuals., Methods: This three-group randomised controlled trial compared the effects of a low-calorie diet (n = 22), a low-calorie diet with chia seeds (30 g/day, n = 22) or a low-calorie diet with concentrated fish oil (1.8 g/day of n-3 long-chain PUFAs, n = 22) in patients with hypertriglyceridaemia. Anthropometrics, fasting blood lipids, proprotein convertase subtilisin/kexin type 9, insulin, adiponectin, leptin and interleukin-6 levels were measured., Results: After 8 weeks, the mean reduction in weight exhibited by the three groups was not statistically different (2.0, 2.7 and 2.8 kg, respectively, for the control, fish oil and chia seed groups). The plasma TG decreased in both the chia seed and fish oil groups in comparison to the control group (p = 0.001). However, no significant difference was observed between the chia seed and fish oil groups (change from baseline mean: 145.2 and 136.7 mg/dL for the chia seed and fish oil groups, respectively). The consumption of chia seeds was associated with a reduction in diastolic blood pressure (change from baseline mean: 8.4 mmHg) compared to the other two groups. No significant alterations were observed in the other blood biochemical factors between the three groups., Conclusions: In people with moderate hypertriglyceridaemia, a low-calorie diet with 30 g of chia seeds compared to fish oil supplements containing 1.8 g of long-chain PUFAs has a similar effect on reducing plasma TG levels, whereas it has a higher blood pressure-lowering effect., (© 2024 British Dietetic Association.)

Purpose: The primary and secondary objectives were to investigate the triglyceride (TG) and LDL-cholesterol (LDL-C) lowering effects of a spread with added plant sterols (PS) and fish oil as compared to a placebo spread., Methods: This study had a randomized, double-blind, placebo-controlled, parallel group design with two intervention arms. Following a 2-week placebo run-in period, 260 healthy individuals with modestly elevated blood TG (≥ 1.4 mmol/L) and LDL-C (≥ 3.4 mmol/L) concentrations consumed either the placebo or intervention spread for 4 weeks. The intervention spread contained 2.0 g/day PS and 1.0 g/day eicosapentaenoic acid (EPA) + docosahexanoic acid (DHA) from fish oil. Fasting serum lipids and apolipoproteins (Apo) (exploratory) were measured at the end of the run-in and intervention phases., Results: Four-week consumption of the intervention spread resulted in significantly lower TG (- 10.6%, 95% CI - 16.0 to - 4.9%; P < 0.001) and LDL-C concentrations (- 5.2%; 95% CI - 7.8 to - 2.4%) as compared to placebo. Total cholesterol (- 3.9%; 95% CI - 6.1 to - 1.5%), non-HDL-C (- 5.4%; 95% CI - 8.1 to - 2.7%), remnant-cholesterol (- 8.1%; 95% CI - 3.4 to - 12.5%), ApoAII (- 2.9%; 95% CI - 5.5 to - 0.2%), ApoCIII (- 7.7%; 95% CI - 12.1 to - 3.1%) and ApoB (- 3.2%; 95% CI - 5.9 to - 0.4%) concentrations were also significantly lower, as compared to placebo. No significant treatment effects were found for HDL-cholesterol, ApoAI, ApoCII, Apo E or ApoB/ApoAI., Conclusions: Four-week consumption of the intervention spread led to significant and clinically relevant decreases in serum TG, LDL-C and other blood lipid concentrations. The study was registered at clinicaltrials.gov (NCT02728583).

Background: Fish oil is known to improve lifestyle-related diseases. These effects occur partly via activation of PPARs by the n-3 polyunsaturated fatty acids included abundantly in fish oil. We investigated fish oil functions on glucose and lipid metabolism that are both dependent on and independent of PPARs pathway., Methods: Mice were fed a diet containing 30 en% beef tallow (B diet) for twelve weeks to induce obesity. The mice were then divided into two groups which were fed either a B diet or a diet containing 30 en% fish oil (F diet). Each group was further divided into two groups which were administered PPARα and γ antagonists or vehicle once a day for three weeks., Results: The F diet groups showed lower triglyceride levels in plasma and liver than the B diet groups, but PPARs antagonists did not affect the triglyceride levels in either diet groups. The F diet groups also showed improvement of glucose tolerance compared with the B diet groups. However, PPARs antagonists made glucose tolerance worse in the F diet group but improved it in the B diet group. Therefore, by the administration of antagonists, glucose tolerance was inversely regulated between the B and F diets, and hypolipidemic action in the plasma and liver of the F diet group was not affected., Conclusion: These results suggest that fish oil decreases lipid levels in plasma and liver via PPARs pathway-independent mechanism, and that glucose tolerance is inversely regulated by PPARs antagonists under diets containing different oils.

Marine omega-3 fatty acids have an important role in reducing the risk of coronary artery disease (CAD). The American Heart Association recommends 1 g/day of omega-3 fatty acids for patients with CAD, and for those without CAD, the consumption of a variety of fish (preferably fatty fish) at least twice a week is recommended. Greater amounts of omega-3 fatty acids (4 g per day) are recommended to treat hypertriglyceridemia. Fish oil capsules are often needed to provide the greater quantities of omega-3 fatty acids necessary to treat hypertriglyceridemia, which should not obscure the important triglyceride-lowering effects of seafood consumption. The effects of fish consumption on plasma lipids and lipoproteins are well described in studies that have generally been conducted with fatty fish and fish oil capsules. This study of a group of men and women in a strictly controlled dietary setting showed that compared with a cholesterol-free diet, both lean fish and beef diets raised plasma low-density lipoprotein cholesterol levels, but the fish diet resulted in lower levels of plasma total cholesterol, very-low-density lipoprotein (VLDL) triglycerides, and VLDL cholesterol, while the beef diet resulted in higher plasma high-density lipoprotein cholesterol levels. These findings can help practitioners to extend their dietary recommendations to incorporate significant quantities of low-fat fish to reduce triglyceride levels.

Hypertriglyceridemia, regarded as one of the independent clinical markers of metabolic syndrome, is a frequently observed disorder that has been shown to be common in the Arab region. Epidemiologic and clinical trials demonstrated that omega-3 fatty acids have the potential to reduce the incidence of cardiovascular disease (CVD); one of the mechanisms by which this effect is achieved is through reducing plasma triglyceride levels. There is strong scientific evidence from human trials that omega-3 fatty acids from either fish or fish oil supplements significantly reduce blood triglyceride levels and these benefits appear to be dose-dependent. The active ingredients of fish oils include the long chain fatty acids EPA and DHA. The ideal amount of omega-3 fatty acid that should be incorporated into the diet without provoking detrimental effects on other lipid components such as decreasing HDL-C and/or increasing LDL-C has not yet been elucidated. Presently, a prescription form of omega-3 fatty acid has been approved by the United States Food and Drug Administration (USFDA) as an adjunct to the diet for the treatment of very high triglyceride levels (> or = 500 mg/dl) in adults. Patients with hypertriglyceridemia have been shown to respond well to the use of omega-3 fatty acids even when used in conjunction with statins where greater improvements in the lipid profile were found as compared to treatment with statins alone. A determinant of the responsiveness to fish oil could be attributed to the ApoE genotype of individuals.

The effects of fish oil on lipoprotein subfractions and low density lipoprotein (LDL) size in non-insulin-dependent diabetes mellitus (NIDDM) patients with hypertriglyceridemia are unknown. To elucidate this, 16 NIDDM hypertriglyceridemic patients (plasma triglyceride 2.25- 5.65 mmol/l, plasma cholesterol < or = 7.75 mmol/l) were randomly assigned to a 6-month period with either moderate amounts of fish oil (n = 8) or placebo (n = 8) after 4 weeks of wash-out and 3 weeks of run-in. Diet and hypoglycemic treatment were unchanged throughout the experiment. LDL size were evaluated at baseline and after 6 months. Three VLDL and LDL subfractions were measured at the end of the two periods. The total lipid concentration of all very low density lipoprotein (VLDL) subfractions was lower at the end of fish oil treatment compared with placebo (large VLDL 124.3 +/- 19.7 mg/dl vs 156.7 +/- 45.5 mg/dl; intermediate VLDL 88.5 +/- 9.5 mg/dl vs 113.9 +/- 23.2 mg/dl; small VLDL 105.9 +/- 9.7 mg/dl vs 128.9 +/- 40.7 mg/dl) (mean +/- SEM), although the difference was not statistically significant. Moreover, at the end of the two treatments, the percentage distribution of VLDL subfractions was very similar (large 37.5 +/- 3.3% vs 37.6 +/- 2.6%, intermediate 27.6 +/- 0.9% vs 31.0 +/- 2.4%; small 34.9 +/- 3.7% vs 31.4 +/- 2.1%). Concerning LDL, no significant change in LDL size was observed after the two treatments (255.4 +/- 2.2 A vs 254.2 +/- 1.7 A, fish oil; 253.7 +/- 2.0 A vs 253.3 +/- 1.7 A, placebo). LDL subfraction distribution was also very similar (large 17 +/- 3% vs 17 +/- 2%; intermediate 62 +/- 3% vs 65 +/- 3%; small 21 +/- 3% vs 18 +/- 2%), at the end of the two periods, confirming the lack of effects on LDL size. In conclusion, our study indicates that in NIDDM patients with hypertriglyceridemia, fish oil does not induce any improvement in LDL distribution and LDL size despite its positive effects on plasma triglycerides.

Early studies in Greenland Eskimos stimulated interest in evaluating the effect of Omega-3 fatty acids on coronary artery disease. Subsequent studies showed a significant decrease in triglyceride levels in patients receiving high doses of fish oil containing DHA and EPA. Slight increases in LDL were also observed in patients receiving fish oil supplements. These studies have also shown a dose-response effect which persists as long as supplementation continues. Later trials, specifically the Diet and Reinfarction Trial and the Indian Experiment of Infarct Survival, have demonstrated a reduction in cardiac death rates and in the incidence of cardiac symptoms in patients receiving fish oil.

We investigated the efficacy of fish oils in Portuguese patients with hypertriglyceridaemia and mixed hyperlipidaemia, and the influence of fish consumption on the triglyceride lowering capacity of fish oils. Forty patients participated in this double-blind study, consisting of a 4-week dietary or wash-out baseline period after which patients were randomly assigned to receive either 12 fish oil capsules (3.6 g/day of omega 3) or similar 12 soya oil capsules per day for a period of 2 months. There were no statistically significant changes of total, HDL or LDL-cholesterol, and triglycerides. Nevertheless, triglycerides increased 19.9% with soya oil and decreased 27.8% with fish oils. Also, there was an inverse relationship (rho = -0.352) between fish consumption and fish oils effect on triglycerides, and the triglyceride lowering with fish oils increased (from 27.8% to 44.4%), reaching borderline significance, if we excluded patients consuming one or more meals with fish per day. Glucose increased 11% (P = 0.0047) with fish oils. These findings suggest that the triglyceride lowering effect of fish oils is affected by fish consumption, and confirm that fish oils increase blood glucose levels in diabetics and non-diabetics.

In the experimental studies reported in this review, dietary n-3 fatty acids from fish and fish oil had profound hypolipidemic effects in normal subjects and in hypertriglyceridemic patients with combined hyperlipidemia (type II-b) and types IV and V hyperlipidemia. In these carefully controlled metabolic experiments, dramatic reductions occurred in plasma triglycerides and to a lesser extent in plasma total cholesterol. Reductions in VLDL, chylomicrons, remnants, LDL, apo B, and apo E were also noted. HDL changes varied from subject to subject. These plasma lipoprotein changes occurred in subjects with non-insulin-dependent diabetes mellitus as well, without deterioration of diabetic control. Similar results are reported in two other papers in this volume. Fish oil did not cause deterioration of diabetic control. Whereas the mechanism of the hypolipidemic action of the n-6 rich vegetable oils containing linoleic acid such as corn or safflower oil still remains obscure, the mechanism of the hypolipidemic action of the n-3 fatty acids in fish oil is well documented. The synthesis of triglyceride and VLDL in the liver is greatly reduced by n-3 fatty acids. At the same time, the turnover of VLDL in plasma is shortened. In another study, LDL production was decreased. Combined with other dietary manipulations, such as a reduction in saturated fat and dietary cholesterol, the use of n-3 fatty acids to treat hyperlipidemia, especially hypertriglyceridemia, appears to have a well-supported rationale. Fish oil combined with a low cholesterol, low saturated fat diet has been shown to produce complementary effects. Total plasma cholesterol and LDL cholesterol were lowered by the low cholesterol, low saturated fat diet, whereas plasma triglyceride and VLDL were decreased by the fish oil. In most situations, the use of fish oil supplements should be regarded as pharmacologic therapy, particularly effective in severe hypertriglyceridemic states (e.g., chylomicronemia). However, a lifelong diet rich in fish may be protective against atherosclerosis as well. Further studies are required to delineate exact doses and precise indications for the use of fish oil in different types of hyperlipidemias and to differentiate the effects, if any, of the two major n-3 fatty acids in fish oil, EPA and DHA. The hypolipidemic effects of n-3 fatty acids coupled with their known antithrombotic actions (secondary to changes in prostaglandin secretion, platelet function, inhibition of growth factors, and enhancement of endothelial-derived relaxation factor) appear to have an important potential role in the control of coronary heart disease and other atherosclerotic disorders. Moreover, fish oil may prevent the "chylomicronemia" syndrome of type V hyperlipidemia.

Background: Because of the inverse relation between dietary fish consumption and coronary heart disease and because of the importance of serum homocysteine as an independent risk factor for atherosclerosis, the effect of fish oil on serum homocysteine was studied in hyperlipemic men., Methods: Fifteen men with either type IIa or IIb lipoproteinemia or hypertriglyceridemia were maintained on a controlled, balanced diet and given either fish oil or olive oil supplements, 12 g/d for 3 weeks, followed by a cross-over period of 3 weeks during which the olive oil or fish oil supplements were given in reverse order. Serum homocysteine was determined by liquid chromatography of acid hydrolyzates of whole serum., Results: Fish oil was found to diminish serum homocysteine levels in 14 of 17 subjects (P < 0.01). Serum homocysteine was 48% +/- 33% less than control values in seven of nine patients and 36% +/- 22% less than values in seven of eight subjects who had first received olive oil. There was no effect of olive oil supplements on serum homocysteine, compared with control values, but olive oil produced an increase in serum homocysteine in those who had first received fish oil. Serum triglycerides and very low-density lipoprotein were decreased by fish oil in patients who were first given olive oil, in agreement with previous studies. There was no effect of either fish oil or olive oil on total cholesterol, apolipoprotein B, low-density lipoprotein, or high-density lipoprotein., Conclusions: The protection against coronary heart disease afforded by a diet rich in fish may be attributed to the lowering of serum homocysteine levels by the n-3 polyunsaturated fatty acids of fish oils.

The clinical efficacy of "Food ichthyenic oil", a new foodstuff, was studied in 129 patients with atherogenic dyslipidemia. The oil was given in a daily dose of 30 ml which contained 8 g polyunsaturated fatty acids of the omega-3 class. All the patients were divided into 3 groups: (1) 44 patients with 5.2-6.5 mmol/l cholesterol; (2) 37 with over 6.5 mmol/l, and (3) 48 with hypercholesterolemia (cholesterol over 5.2 mmol/l and hypertriglyceridemia (triglycerides over 2.3 mmol/l). Following 1-month therapy, all the groups displayed lower low density lipoprotein cholesterol levels and significantly higher high density lipoprotein cholesterol concentrations. After 4-month intake of ichthyenic oil, the levels of total and LDL cholesterol returned to the baseline values, whereas the concentration of HDL cholesterol was significantly higher than the baseline one. Following 12-month therapy, there were 15 and 14% decreases in total and LDL cholesterol, respectively, a 16% increase in HDL cholesterol. The patients from Group 3 exhibited low VLDL cholesterol and triglyceride levels.

Dietary n-3 fatty acids (FAs) found in fish oils markedly lower plasma triglyceride (TG) and very low density lipoprotein (VLDL) levels in both normal and hypertriglyceridemic subjects. The present study examined the mechanism of this effect. Ten subjects with widely different plasma triglyceride levels (82 to 1002 mg/dl) were fed metabolically controlled diets containing 20% fat. The control diet contained a blend of cocoa butter and peanut oil (P/S = 0.8). The test diet contained fish oil (P/S = 1.1) and provided 10-17 g of n-3 FAs per day (depending on calorie intake). After 3 to 5 weeks of each diet, the kinetics of VLDL-TG were determined over a 48-h period after the injection of [3H]glycerol. The fish oil diet reduced the VLDL-TG synthetic rate from 23 +/- 14.3 (mean +/- SD) to 12.6 +/- 7.5 mg/h per kg ideal weight (P less than 0.005) and increased the fractional catabolic rate (FCR) for VLDL-TG from 0.23 +/- 0.12 to 0.38 +/- 0.16 h -1 (P less than 0.005). At the same time, there was a 66% reduction of plasma triglyceride levels, resulting largely from a 78% decrease in VLDL-TG levels (398 +/- 317 to 87 +/- 77 mg/dl; P less than 0.005). There was a strong correlation (r = 0.83; P less than 0.01) between the change in synthetic rates and pool sizes, but there was no correlation (r = 0.24; NS) between changes in FCRs and pool sizes. The VLDL cholesterol: triglyceride ratio increased during the n-3 diet suggesting that smaller VLDL particles were present. These particles would be expected to leave the VLDL fraction more rapidly than larger particles producing a higher FCR. We conclude that the hypotriglyceridemic effect of fish oil appears to be caused primarily by an inhibition of very low density lipoprotein-triglyceride synthesis, but an additional, independent effect upon VLDL catabolism cannot be ruled out.

Study Objective: To determine whether high doses of fish oil concentrate followed by low-dose maintenance therapy can sustain the initial plasma triglyceride reductions., Design: Before-and-after trial with 3-month treatment periods., Setting: Outpatient lipid clinic at a university medical center., Patients: Sixteen patients with hypertriglyceridemia recruited from the General Internal Medicine Clinics. Five had concomitant hypercholesterolemia (type IIb)., Intervention: Fish oil supplementation at two doses. After basal measurements, 9.8 g/d omega-3 fatty acids were provided for study months 1 to 3, and 3.9 g/d were provided for study months 4 to 6., Measurements and Main Results: Blood was drawn monthly and plasma was analyzed for levels of triglycerides, low-density-lipoprotein (LDL) cholesterol and apolipoprotein B, high-density-lipoprotein (HDL) cholesterol and apolipoprotein A1, and glucose and glycohemoglobin. During therapy with the higher dose, mean plasma triglyceride levels were reduced from 3.65 +/- 0.35 mmol/L at baseline to 1.85 +/- 0.20 mmol/L at 1 month, but increased by 30% to 2.40 +/- 0.30 mmol/L by the third month of therapy (P less than 0.05): this increase could not be explained by changes in body weight or compliance. Plasma triglyceride levels continued to increase with low-dose therapy and remained only 11% below baseline values by the sixth month of therapy (P = not significant). Although fish oil therapy increased HDL cholesterol levels (+18% at high dose; 99% CI, 5% to 31%), favorable changes were not seen in LDL cholesterol, apolipoprotein B, or apolipoprotein A1 levels., Conclusions: Fish oil concentrate at high doses followed by low-dose maintenance therapy cannot sustain the initial large plasma triglyceride reductions. Moreover, the efficacy of the higher dose becomes less pronounced after the first month of therapy. This reduced efficacy during prolonged therapy, and the lack of beneficial effect on apolipoprotein and LDL cholesterol levels, may limit the practical benefit of fish oil in the treatment of hypertriglyceridemia.

The presence of fish oils in a background diet appears to reduce postprandial triglyceridemia from a fatty test meal.

Unlike the well-established hypotriglyceridemic effect of omega-3 fatty acid supplementation, the influence of more clinically tolerable doses on lipoproteins and apolipoproteins is less well characterized. Therefore, we compared the relative effects of modest doses of omega-3 fatty acid supplementation with a corn oil control on lipids, lipoproteins, and apolipoproteins in a randomized, double-blind controlled crossover study. Eight hypertriglyceridemic subjects ingested 4.6 g/d of omega-3 fatty acids or 5.4 g/d of linoleic acid (supplied as corn oil) for 8 weeks, then crossed over to the alternative encapsulated oil for another 8 weeks, following an interposed 4-week wash-out period. Compared with the corn oil control, fish oil supplementation caused a significant reduction in triglyceride levels by a mean of 2.21 mmol/L and increased the high-density lipoprotein cholesterol by a mean of 0.13 mmol/L, associated with a significant rise in the high-density lipoprotein 3 subfraction. Furthermore, there was a significant increase in low-density lipoprotein (LDL) apolipoprotein B levels by a mean of 0.246 g/L. Compared with corn oil, no statistically significant change for LDL cholesterol or other apolipoprotein levels occurred, although LDL cholesterol showed a mild elevation. These data suggest that unlike large doses of omega-3 fatty acids, the hypotriglyceridemic effect of modest amounts of encapsulated fish oil supplementation is unaccompanied by favorable changes in LDL cholesterol or LDL apolipoprotein B levels; the potential therapeutic usefulness of modest doses of dietary fish oil for the treatment of hypertriglyceridemia, therefore, may be limited.