Why omega-3 are algal molecules

Salmon, sardines and cod are not the source of omega-3; they are concentrators of it, one trophic level up the same chain. EPA and DHA are made at the bottom of the marine food web, by microalgae and their relatives, which is why an industry that wants fish oil without fish ends up growing algae instead.

Cold water demands flexible membranes

Membranes stiffen as temperature falls, and a stiff membrane fails at its job of transport and signaling. The algal solution is chemistry: fatty acids with several double bonds — EPA, DHA — have kinked tails that stay fluid in the cold, so cold-water algae pack them into their chloroplast and cell membranes. The double bonds are installed by desaturase enzymes working stepwise with elongases, extending and unsaturating shorter chains; this is the aerobic route, dependent on oxygen and found across phototrophs such as Nannochloropsis, whose EPA sits mostly in its chloroplast galactolipids. A second, independent solution exists: some heterotrophic microalgae — Schizochytrium, Crypthecodinium — build DHA with a large polyketide-synthase-like enzyme that needs no oxygen at all, which is the reason these species ferment so well in the dark. That both routes arrive at the same molecules is convergence; the industrial significance is that the second route unties lipid production from light entirely.

Getting the lipid out of the cell

The oil does not sit in a free pool. In phototrophs much of the EPA is structural — bound into membrane lipids — while storage oil accumulates as triacylglycerol droplets. Either way, the lipid is behind a cell wall, and extraction begins with disruption: mechanical bead milling, high-pressure homogenization or enzymatic weakening, each costing energy against a wall evolved to keep things out. Recovery then runs by solvent or supercritical carbon dioxide, and the split between polar membrane lipids and neutral storage oil matters commercially: an EPA product delivered as phospholipids or glycolipids is a different extraction and a different absorption profile than a triglyceride oil.

Oxidation is the limiting process

Polyunsaturated fatty acids are reactive by design: the same double bonds that keep membranes fluid are attack sites for oxygen. Autoxidation starts with abstraction at an allylic position and runs as a chain reaction producing peroxides, aldehydes and rancid flavors; DHA, with six double bonds, is among the more oxidation-prone lipids in food. Everything downstream is therefore an oxygen-avoidance exercise — processing under nitrogen, low temperatures, antioxidants such as tocopherols — and a genuine tension sits in refining: deodorization removes off-flavors but also strips the natural antioxidant fraction. Peroxide and anisidine values are the honest scoreboard of the trade, because oxidation is not a quality defect that might appear — it is the default direction of the chemistry, and shelf life is simply the time bought against it.