Description
Omega 620 Mg Tablets – Omega-3 Fatty Acids 620 mg
Omega 620 Mg Tablets contain omega-3 fatty acids 620 mg, a concentrated marine lipid formulation providing the two principal long-chain polyunsaturated fatty acids of therapeutic importance: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These essential fatty acids cannot be synthesised in adequate quantities by the human body and must be obtained through diet or supplementation.
Omega-3 fatty acids exert broad cardioprotective and metabolic benefits, most significantly a substantial reduction in elevated plasma triglyceride levels. At therapeutic doses, they are indicated as adjunctive therapy to diet and statin treatment in patients with hypertriglyceridaemia and are associated with reduced cardiovascular risk in patients with established coronary artery disease.
Mechanism of Action
The therapeutic effects of EPA and DHA operate through multiple complementary mechanisms:
- Triglyceride reduction: EPA and DHA reduce hepatic triglyceride synthesis by inhibiting diacylglycerol acyltransferase and other enzymes in the triglyceride synthesis pathway; they also increase β-oxidation of fatty acids in the liver and enhance clearance of VLDL (very-low-density lipoprotein) particles from plasma by upregulating lipoprotein lipase activity. At prescription doses, omega-3s reduce fasting triglycerides by 20–50% in patients with hypertriglyceridaemia
- Anti-inflammatory effects: EPA and DHA are precursors to specialised pro-resolving lipid mediators — resolvins, protectins, and maresins — which actively resolve inflammation by reducing neutrophil trafficking, promoting macrophage clearance of inflammatory debris, and suppressing NF-κB-mediated inflammatory cytokine production. DHA-derived docosanoids reduce inflammatory gene expression in endothelial cells
- Antiplatelet and vascular effects: Omega-3s reduce thromboxane A₂ production (a potent platelet aggregation promoter) and increase prostacyclin (PGI₂) synthesis (a vasodilator and platelet aggregation inhibitor), resulting in a mild antiplatelet and vasodilatory effect
- Membrane incorporation and cardiac electrophysiology: EPA and DHA incorporate into cell membrane phospholipids, altering membrane fluidity and ion channel function. DHA’s incorporation into cardiac membrane phospholipids is associated with reduced cardiomyocyte excitability and reduced risk of ventricular arrhythmias
- Blood pressure: Modest antihypertensive effect (~2–4 mmHg reduction in systolic blood pressure) in hypertensive patients, mediated through improved nitric oxide bioavailability and reduced production of vasoconstrictors
Indications
- Hypertriglyceridaemia: As an adjunct to diet in patients with severe hypertriglyceridaemia (fasting triglycerides ≥500 mg/dL); also used in combination with statins for mixed dyslipidaemia
- Secondary prevention of cardiovascular disease: In patients with a history of myocardial infarction; evidence from trials supports reduction in cardiovascular mortality and sudden cardiac death
- Adjunctive nutritional support: In conditions associated with omega-3 deficiency including malabsorption syndromes, restricted diets, and certain hepatic conditions
- Non-alcoholic fatty liver disease (NAFLD): Adjunctive therapy to improve hepatic steatosis and liver function parameters
- Inflammatory conditions: Adjunctive support in rheumatoid arthritis (reduces tender joint count and morning stiffness), inflammatory bowel disease, and other chronic inflammatory conditions
Dosage and Administration
- Standard dose (supplementation): 1–2 tablets daily with food
- Therapeutic dose (hypertriglyceridaemia): 2–4 g of EPA+DHA daily (dose titrated to response), with or after meals; take with food to maximise absorption and reduce GI side effects (fishy aftertaste, belching)
- Swallow tablets whole; do not crush or chew
- Consistency of daily use is important for sustained triglyceride-lowering effect
- Refrigerating softgel or oil-based omega-3 formulations reduces fishy aftertaste and oxidation
Pharmacokinetics
Omega-3 fatty acids are absorbed in the small intestine as free fatty acids and monoglycerides following hydrolysis by pancreatic lipase. Absorption is enhanced when taken with a fat-containing meal. Fatty acids are incorporated into chylomicrons and transported via the lymphatic system into the systemic circulation.
EPA and DHA undergo rapid and extensive incorporation into plasma and cellular membrane phospholipids. Plasma half-life following a single dose is approximately 1–2 days for EPA and 2–5 days for DHA. With regular supplementation, red blood cell membrane EPA and DHA levels (the omega-3 index) reach a new steady state within 4–8 weeks, reflecting tissue incorporation. EPA is partly retroconverted to DHA; both are ultimately metabolised to prostanoids, resolvins, and other oxygenated derivatives, then excreted via oxidative pathways.
Clinical Evidence
Major randomised controlled trials have established omega-3 fatty acids as a cornerstone of cardiovascular risk reduction:
- GISSI-Prevenzione (1999): 1 g/day omega-3 reduced total mortality by 20% and sudden cardiac death by 45% in post-MI patients over 3.5 years
- REDUCE-IT (2018): High-dose icosapentaenoic acid (EPA) 4 g/day (as icosapent ethyl) reduced major adverse cardiovascular events by 25% in statin-treated patients with elevated triglycerides and established cardiovascular disease or diabetes
- JELIS (2007): EPA supplementation significantly reduced major coronary events in Japanese patients with hypercholesterolaemia
These findings underpin current guidelines recommending omega-3 supplementation as adjunctive cardiovascular risk reduction, particularly in patients with persistently elevated triglycerides despite statin therapy.
Contraindications
- Known hypersensitivity to omega-3 fatty acids, fish, fish oil, or any excipient in the formulation
- Allergy to soy (some formulations contain soya lecithin)
- Pregnancy and breastfeeding — high-dose pharmaceutical omega-3 formulations (not dietary supplements) should only be used under medical supervision
Precautions and Warnings
- Anticoagulant and antiplatelet effects: Omega-3s have mild antiplatelet activity. Patients on warfarin or antiplatelet drugs (aspirin, clopidogrel) should be monitored; at standard supplemental doses the clinical risk of bleeding is low but increases at higher therapeutic doses
- Fish allergy: As omega-3 preparations are derived from marine sources, use with caution in patients with fish or shellfish allergy
- LDL-cholesterol: At very high doses, omega-3s may modestly increase LDL-C in some patients; monitor lipid profiles in patients being treated for dyslipidaemia
- Atrial fibrillation: Some data suggest that high-dose omega-3 supplementation may be associated with a small increase in atrial fibrillation risk in certain populations; discuss with a physician before high-dose use in patients with AF risk factors
- Glycaemic control: Generally not affected at standard doses; monitor in patients with type 2 diabetes at higher therapeutic doses
Drug Interactions
- Warfarin and anticoagulants: High-dose omega-3s can enhance anticoagulant effect; monitor INR when starting or changing omega-3 doses
- Antiplatelet drugs (aspirin, clopidogrel, ticagrelor): Additive antiplatelet effect; relevant at high doses
- Statins: No pharmacokinetic interaction; combined use is safe and complementary — statins primarily reduce LDL while omega-3s primarily reduce triglycerides
Adverse Effects
- Common: Fishy breath or aftertaste (most common complaint), belching, nausea, dyspepsia, diarrhoea — particularly at higher doses; reduced by taking with food
- Uncommon: Mild transient bleeding (nosebleeds, bruising at high doses), rash, pruritus
- Rare: Allergic reactions; mild transaminase elevation at high doses
Storage Instructions
- Store below 25°C in a cool, dry place away from direct light
- Keep the container tightly closed after each use
- Refrigeration may help reduce fishy odour in liquid or softgel formulations
- Keep out of reach of children
- Do not use after the expiry date
Frequently Asked Questions
What is the difference between Omega 620 and Omega S 620?
Omega S 620 contains omega-3 fatty acids with an additional supplementary component, while Omega 620 provides omega-3 fatty acids only. Your doctor will select the formulation appropriate to your treatment needs.
Can Omega 620 replace my statin for cholesterol?
No. Statins primarily lower LDL (bad) cholesterol, while omega-3s primarily lower triglycerides. They act through different pathways and are often used together. Omega-3s do not replace statin therapy.
How long before Omega 620 shows results?
Triglyceride-lowering effects typically begin within 2–4 weeks of regular use. Full benefit on cardiovascular risk markers takes several months of consistent supplementation. The omega-3 index in red blood cell membranes reaches a new steady state in 4–8 weeks.
Can Omega 620 be taken safely with blood thinners?
At standard supplemental doses, the antiplatelet effect of omega-3s is mild and generally safe. At higher therapeutic doses (≥3 g/day), inform your doctor and monitor your anticoagulation status if you are taking warfarin or other blood thinners.
References
- U.S. Food and Drug Administration. Lovaza (omega-3-acid ethyl esters) capsules – prescribing information. Available at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/021735s036lbl.pdf
- National Library of Medicine – DailyMed. Omega-3-acid ethyl esters – drug information. Available at: https://dailymed.nlm.nih.gov/dailymed/search.cfm?labeltype=all&query=omega-3+acid+ethyl+esters
- Bhatt DL, et al. Cardiovascular risk reduction with icosapentaenoic acid for hypertriglyceridaemia (REDUCE-IT). N Engl J Med. 2019;380(1):11–22.
- GISSI-Prevenzione Investigators. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction. Lancet. 1999;354(9177):447–455.

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