This article is for educational purposes only. It's not medical advice. Talk to a healthcare provider before making changes to your diet or health routine.

Quick Answer

Omega-3 and omega-6 are essential polyunsaturated fats your body can't synthesize. EPA and DHA (marine omega-3s) have strong evidence for cardiovascular and anti-inflammatory benefits. Plant-based omega-3 (ALA) converts to EPA and DHA poorly, making fatty fish or algae-based supplements the most reliable source. The omega-6 to omega-3 ratio debate is real but secondary to simply getting adequate EPA and DHA.

The Science

Some nutrients are optional. Your body makes them if you don’t eat enough. Omega-3 and omega-6 fatty acids aren’t in that category. They’re called essential fatty acids because your body can’t synthesize them from scratch. You have to eat them.

Both are polyunsaturated fats (PUFAs). “Polyunsaturated” means the carbon chain has multiple double bonds, which is what makes them liquid at room temperature and reactive to heat and light. “Essential” means dietary requirement, not that one is more important than the other.

The story gets more complicated when you look at what your body actually does with these fats, because not all omega-3s are created equal.

The Omega-3 Family: ALA, EPA, and DHA

There are three main omega-3 fatty acids:

ALA (alpha-linolenic acid) is the plant-based form. It’s found in flaxseed, chia seeds, hemp seeds, walnuts, and some plant oils. ALA is the omega-3 you get most of if you eat a plant-based diet without supplements.

EPA (eicosapentaenoic acid) is the marine form with the strongest anti-inflammatory signaling evidence. It’s found in fatty fish, shellfish, and algae.

DHA (docosahexaenoic acid) is the marine form most concentrated in the brain and retina. It’s key for brain development during pregnancy and infancy, and plays a structural role in neural tissue throughout life.

Your body can technically convert ALA into EPA and then DHA. The conversion pathway exists. The problem is efficiency.

Research consistently shows that the conversion of ALA to EPA is roughly 5-15% in healthy adults, and conversion to DHA is far lower, often under 1% (Burdge and Calder, 2005, Proceedings of the Nutrition Society). This is like trying to fuel a car by converting rainwater to gasoline. The process is technically possible. The yield is too low to rely on.

This is why dietary sources or supplements that provide EPA and DHA directly are the most reliable way to raise blood levels of these fatty acids. Algae are where fish get their EPA and DHA in the first place. Fish don’t synthesize it themselves. So algae-based supplements bypass the conversion problem entirely and are the most direct plant-based route.

The Omega-6 Family

The primary omega-6 is linoleic acid (LA), found in most vegetable oils: corn oil, sunflower oil, soybean oil, safflower oil. LA is abundant in the modern diet.

Your body can convert LA to arachidonic acid (AA), which is a precursor to certain signaling molecules including some prostaglandins and leukotrienes involved in inflammation. This is the basis for the claim that omega-6 fats are “pro-inflammatory.”

But the biochemistry is more complicated than that framing. LA itself appears to have neutral or anti-inflammatory effects in most contexts. Clinical trials replacing saturated fat with omega-6 fats have generally shown cardiovascular benefits, not harm (Mozaffarian et al., 2010, PLOS Medicine). The conversion from LA to AA is also regulated by the same set of enzymes that convert ALA to EPA and DHA, meaning the two pathways compete.

The Ratio Hypothesis

Here’s where things get contested.

Researchers have observed that the ratio of omega-6 to omega-3 in the modern diet has shifted dramatically. Evolutionary estimates suggest our ancestors ate diets with an omega-6 to omega-3 ratio close to 4:1. Current Western diets average around 15:1 to 20:1, primarily because vegetable oil consumption has increased and fatty fish consumption is relatively low (Simopoulos, 2002, Biomedicine and Pharmacotherapy).

Some researchers argue this ratio shift is itself a health problem. The excess of omega-6 competes with omega-3 for the conversion enzymes and promotes an inflammatory state.

The ratio hypothesis is plausible but not firmly established. The challenge is distinguishing between two explanations:

  1. The ratio itself matters (high omega-6 actively harms when omega-3 is low)
  2. The absolute amount of omega-3 is what matters (you’re just not getting enough EPA and DHA)

Clinical trials testing these hypotheses haven’t cleanly separated them. But current evidence suggests that raising omega-3 intake (rather than reducing omega-6) is the more effective intervention for cardiovascular and inflammatory markers (Harris, 2006, Prostaglandins, Leukotrienes and Essential Fatty Acids).

In practical terms: don’t worry about eliminating olive oil or nuts because they contain omega-6. Focus on getting adequate EPA and DHA.

A closer look: The omega-3 cardiovascular evidence, where it's strong and where it isn't

The history of omega-3 cardiovascular research is a useful case study in how evidence evolves.

Early evidence was compelling. Observational research found that Greenlandic Inuit populations eating diets very high in marine fats had exceptionally low rates of cardiovascular disease. The DART trial in 1989 found that advising men who had survived heart attacks to eat fatty fish twice a week reduced mortality by 29%.

This led to widespread recommendation of fish oil supplements. But large randomized controlled trials have produced more mixed results.

The ASCEND trial (2018) tested omega-3 supplementation in people with diabetes but without cardiovascular disease. It found a modest reduction in serious vascular events that wasn’t statistically significant for its primary outcome. The VITAL trial (2019) in healthy adults found no significant reduction in major cardiovascular events from fish oil supplementation.

But then: the REDUCE-IT trial (2018) using high-dose icosapentaenoic acid (EPA only, at 4g/day, far higher than standard supplement doses) in people with elevated triglycerides found a 25% relative reduction in cardiovascular events. This generated significant excitement. It also generated controversy: critics noted that the control group used mineral oil, which may have worsened cardiovascular outcomes, inflating the apparent benefit.

Where does this leave us?

  • Strong evidence: omega-3 supplementation reduces triglycerides (by 15-30% at doses of 2-4g/day). This is well established.
  • Good evidence: omega-3 from food (fatty fish) is associated with lower cardiovascular risk in prospective studies.
  • Moderate evidence: high-dose EPA supplementation may benefit people with elevated cardiovascular risk and high triglycerides.
  • Mixed evidence: standard-dose fish oil for primary prevention in otherwise healthy people.

The evidence is strongest for people with existing cardiovascular disease or elevated triglycerides, and weakest for healthy people hoping to prevent a first event.

Food Sources: How to Get Enough

FoodServingEPA + DHA
Atlantic salmon (farmed)3 oz cooked~1,800mg
Sardines (canned in oil)3 oz~1,350mg
Mackerel (Atlantic)3 oz cooked~1,000mg
Rainbow trout (farmed)3 oz cooked~900mg
Albacore tuna (canned)3 oz~730mg
Algae-based DHA supplementvaries by brand200-500mg DHA
Flaxseed oil1 tbsp~7,260mg ALA (poor EPA/DHA conversion)

Two servings of fatty fish per week (the recommendation from the American Heart Association and most major health bodies) provides roughly 500mg EPA+DHA per day on average. That meets the needs of most healthy adults.

Fish Oil Quality

Not all fish oil supplements are equal. Omega-3 fatty acids are highly unsaturated fats, which means they’re prone to oxidation and going rancid. Studies have found that a significant proportion of commercial fish oil supplements contain oxidized lipids, which may reduce or reverse any benefit (Jackowski et al., 2015, Journal of Nutritional Science).

Signs of rancidity include a fishy or paint-like smell when the capsule is cut open. Quality markers include third-party testing (IFOS certification), storage in dark containers, and inclusion of vitamin E (tocopherols) as an antioxidant.

Algae-based supplements avoid this problem to some extent because algae oils don’t go rancid as quickly as fish oils. They also avoid concerns about contaminants like mercury and PCBs that can concentrate in larger fish.

Cooking Considerations

How you cook fatty fish matters. High-heat methods like grilling at very high temperatures can oxidize delicate omega-3 fats. Gentler methods (poaching, baking, or cooking at lower temperatures) preserve more of the EPA and DHA content. This intersects with the smoke point discussion for cooking oils. The cooking science guide on smoke points covers how heat affects different fats in the cooking context.

The bottom line is straightforward: EPA and DHA from marine sources have the strongest evidence, plant-based ALA doesn’t convert reliably, and getting two servings of fatty fish per week is a reasonable, evidence-supported target for most people.

What This Means for You

Eating fatty fish (salmon, sardines, mackerel, trout) twice a week meets most people's EPA and DHA needs. If you don't eat fish, algae-based DHA/EPA supplements are the most direct alternative. They're more effective than flaxseed oil because ALA conversion is too low to reliably raise blood EPA and DHA. Focus on getting enough EPA and DHA rather than obsessing over your omega-6 to omega-3 ratio.

References

  1. Burdge GC, Calder PC. (2005). Conversion of alpha-linolenic acid to longer-chain polyunsaturated fatty acids in human adults. Reproduction Nutrition Development. 45(5):581-97.
  2. Mozaffarian D, Micha R, Wallace S. (2010). Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLOS Medicine. 7(3):e1000252.
  3. Simopoulos AP. (2002). The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomedicine and Pharmacotherapy. 56(8):365-79.
  4. Harris WS, Assaad B, Poston WC. (2006). Tissue omega-6/omega-3 fatty acid ratio and risk for coronary artery disease. American Journal of Cardiology. 98(4A):19i-26i.
  5. Jackowski SA, Alvi AZ, Mirajkar A, et al. (2015). Oxidation levels of North American over-the-counter n-3 (omega-3) supplements and the influence of supplement formulation and delivery form on evaluating oxidative safety. Journal of Nutritional Science. 4:e30.