Two fatty acids the body cannot make
Essential, and that is meant literallyThe human body builds almost every fatty acid it needs. Two families are the exception : omega-3 and omega-6. It lacks the enzymes to place a double bond at those positions, so both have to come from food. That is what makes them essential, in the strict sense of the word rather than the marketing one.
The interesting part is not that they are needed. It is where they end up : not as fuel, but built into the membrane of every cell. A fatty acid in a membrane is not a store of energy. It is part of the structure, and structure determines behaviour.
ALA, EPA and DHA : why the plant route is limited
Three names, one chainOmega-3 is not one substance. Three matter in practice, and they are not equivalent.
ALA from plants
Alpha-linolenic acid is found in linseed oil, walnuts and rapeseed oil. It is the only omega-3 fatty acid the body strictly has to take in ; in theory the body builds the longer ones from it.
Conversion to EPA
The conversion runs through the same enzymes that the omega-6 fatty acids compete for. In adult humans the yield is low and varies considerably between individuals and sexes.
On to DHA
The final step is the weakest. In practice, therefore, how much DHA ends up in membranes depends less on plant intake than on taking in EPA and DHA directly.
The size of that limitation has been examined directly in adults, and the review of those studies is unambiguous : the conversion from ALA onward is limited, the step to DHA in particular (Burdge, Reprod Nutr Dev 2005, PMID 16188209). This is the reason a diet rich in linseed oil is not automatically a diet rich in DHA. It is also the reason the question 'how much omega-3 do you eat?' is less useful than it sounds.
Why the red blood cell gets measured
Membrane instead of plasmaFatty acids can be measured in plasma, and that measurement mostly reports what was eaten recently. The membrane of the red blood cell behaves differently. It is built once, when the cell is formed, and then carries that composition for its whole life of roughly four months. What is measured there is therefore not yesterday's meal but the supply over the preceding weeks.
That is the whole idea behind the omega-3 index, and it was introduced with exactly this rationale : a membrane-based measure that does not jump around with the last meal (Harris and von Schacky, Prev Med 2004, PMID 15208005). It is a rare case where the choice of sample material is the actual innovation, not the analysis.
What a fatty acid does inside a membrane
Structure becomes functionA membrane is not a wall but a fluid layer, and how fluid it is depends on the fatty acids in it. Long chains with many double bonds, which is exactly what EPA and especially DHA are, bend and cannot pack tightly. Membranes containing a lot of them stay more mobile. Proteins sitting in such a membrane, ion channels and receptors among them, are not floating in a neutral medium. Their surroundings shape how they move and therefore how they work.
This is the part that is easy to overstate. That membrane composition influences the behaviour of embedded proteins is well established. That a particular reading in a blood test therefore changes a particular function in a particular person rests on a much longer chain of inference, and most of the popular claims quietly skip its middle.
The resolution phase : inflammation is ended, not suppressed
The most interesting mechanism hereFor decades the end of an inflammation was treated as what happens when the trigger runs out. That picture turned out to be wrong. Ending an inflammation is its own programme, with its own signalling molecules, and it is switched on deliberately. These molecules were given a name of their own : specialised pro-resolving mediators (Serhan, Nature 2014, PMID 24899309).
Their raw material is EPA and DHA. From them the body forms resolvins, protectins and maresins, and these do something different from an anti-inflammatory drug. They do not block the inflammatory signal. They actively bring the episode to a close : they stop further immune cells being called in, they get the ones already present to clear away debris and dead cells, and they return the tissue to its normal state (Serhan, Cold Spring Harb Perspect Biol 2014, PMID 25359497).
The distinction matters more than it first appears. Suppressing inflammation and resolving it are not two words for the same thing. A suppressed inflammation is one whose signal has been turned down ; a resolved one is finished, with the tissue cleaned up. That the body does not make this raw material itself but has to take it in is the reason the field is studied at all. Whether additional intake measurably changes the process in humans is a different question.
Not every tissue takes up the same amount
Brain, muscle and blood differIncorporation is not uniform. Nervous tissue and the retina hold a strikingly high share of DHA, and they hold on to it : their composition changes slowly and reluctantly. Muscle and blood cells exchange their fatty acids more readily. That has a practical consequence for interpretation. A measurement in blood describes the blood, and how well it stands in for a given tissue differs from tissue to tissue.
So far the mechanism. Now the part that concerns you.
From mechanism to valueEverything above describes how the system works. None of it tells you what your own reading means, which of the two fatty acids matters for what, or what the randomised trials found when this was actually tested. That last point is where the comfortable story and the evidence part company.
The rest is for clients.
Up to this point the article covers the mechanism. What follows moves from the mechanism to your own values, and that part we keep for the people we work with.
- EPA and DHA are not interchangeable : where the paths diverge, and why that matters when reading a trial
- What the randomised evidence supports : two negative individual trials, a pooled analysis of 13 trials pointing the other way, and how the two fit together
- The dose-dependent counter-signal that argues against the idea that more is automatically better
- Muscle and brain : why we cite nothing here even though a literature exists
- Why the measure works as a marker, where its limit sits, and how our target value came about, decided rather than guessed
There is no self-service sign-up. Access comes with working together ; the first conversation is free and non-binding.
This article is educational and does not replace medical advice. StoaVita provides longevity and performance consulting, not medical treatment, and makes no individual dosing recommendations. If your reading falls outside the usual range, please have it assessed by a doctor. Regardless of your own reading : an intake above roughly one gram of EPA and DHA per day belongs in a conversation with your doctor beforehand, because the risk of atrial fibrillation rises with dose. That is not an all-clear for anything below it : it is the point beyond which we stop answering the question, not the point beyond which it becomes unsafe. Anyone already taking more should not change it in either direction on their own while under medical treatment. This applies in particular alongside anticoagulant medication, ahead of planned surgery, and with a current or past rhythm disturbance.
Measure instead of guess
The omega-3 index is one marker among roughly 70 to 100 in the Longevity Check-up. Interpreted in context, not in isolation.