The conversion step horses depend on, and why it often falls short

New here? Our guide to omega-3 for horses sets out what the feeding trials found →

When omega-3 is fed as ALA, the body has a job to do before it can use it, and the previous article in this series established what that job is: ALA is a short-chain omega-3, a building block that has to be converted into EPA and DHA before those molecules can do anything useful in the tissues.

This post looks at what happens when horses are actually fed ALA and someone measures the result. We are going to start with the measurements and come to the explanation afterwards, because the measurements are the part we are most sure of and the explanation is the part we are least sure of.

What the horse studies found

In a 90-day controlled study, mares were fed one of three diets: no supplement, an omega-3 supplement supplying EPA and DHA, or flaxseed meal supplying exactly the same quantity of omega-3 in the form of ALA. Both supplemented groups therefore received the same amount of omega-3, differing only in the form it arrived in.

Red blood cell EPA and DHA were detected only in the group receiving EPA and DHA directly, where EPA rose by 38% between days 30 and 60 and DHA by 56% between days 30 and 90. The flaxseed group showed no such rise at all.¹

An earlier study in yearlings fed either fish oil or milled flaxseed found something consistent with this. The flaxseed group did show a rise in circulating ALA at day 35, so the ALA was clearly being absorbed, but that rise was not sustained and by day 70 it had returned to where it started, with the long-chain omega-3s never accumulating.²

Why the blood and the membrane are different questions

You will sometimes read that ALA supplementation does raise omega-3 levels in horses, which is not necessarily wrong, and it is worth understanding how both things can be true at once.

A fatty acid can appear in plasma, circulating in the blood, without ever being incorporated into cell membranes. Plasma gives you something closer to a picture of what the horse ate recently, whereas the membrane gives you a picture of what the horse is built from — and it is the membrane that matters here, because that is where EPA and DHA sit until the body needs them.

Both of the studies above measured red blood cell membranes rather than plasma alone, which is a harder test and a considerably more useful one.

What conversion involves

The horse eats ALA — from grass, from linseed, from any plant source — as an 18-carbon chain, while EPA has 20 carbons and DHA has 22. Getting from one to the other means the body has to extend and modify that chain step by step, with each step handled by a specific enzyme.

It works rather like a production line, where ALA arrives at the start, each station performs one job, and by the end, if everything has gone to plan, the body has produced EPA and then DHA. The enzyme that starts that line is called delta-6 desaturase, and because it performs the first step, nothing downstream happens without it.

The leading explanation

Here is where we move from measurement to interpretation, and we want to be clear about which of the two you are reading.

Delta-6 desaturase is not dedicated to omega-3, because the same enzyme is also needed to process omega-6 fatty acids, the other major family of polyunsaturated fats, so both families end up queuing for the same station on the production line.

What decides the outcome is not that the enzyme prefers one family over the other, but the ratio in which they arrive. Work using labelled fatty acids in human liver cells found that the conversion of ALA into EPA and DHA depended on the ratio of omega-6 to omega-3 supplied, so that changing the ratio changed how much conversion took place. Where a diet supplies omega-6 in large excess, omega-3 conversion is reduced — not because the body has chosen badly, but because it has been outnumbered.³

Where that explanation runs out

Two things are worth being straight about. The mechanism has been characterised in rats, in human cell lines and in other species but not in the horse, and expecting the horse to work similarly is not the same as having shown that it does. More awkwardly, if omega-6 competition were the whole story then conversion ought to work reasonably well in horses whose diets are not high in omega-6 — yet the yearlings had free access to growing pasture, where ALA is the dominant fatty acid, and flaxseed still failed to produce a sustained result.

Competition is therefore a plausible contributing factor borrowed from work in other species rather than a complete account, and something else appears to be limiting the pathway in the horse that nobody has yet identified.

Why outcomes vary between horses

One of the more frustrating aspects of ALA-based supplementation is how inconsistent the outcomes are, with the same product at the same dose appearing to do something in one horse and nothing obvious in another.

Several things could plausibly drive that variation, including the omega-6 to omega-3 ratio of the wider diet, the metabolic state of the horse, and individual differences in how much of the enzyme is available — all three of which influence conversion in other species.^{3 5}

We would be overstating it to present these as established explanations for variation between horses, because they are candidates rather than findings. What is established is the variation itself, and the fact that you cannot see it from the outside: two horses on identical supplementation may be producing very different amounts of EPA and DHA internally, and nothing on the feed label tells you which horse you have.

The implication

If the constraint sits in the conversion step itself, then feeding more ALA does not obviously fix it, because the production line has a capacity limit and pushing more raw material into it does not expand that capacity. Whatever is limiting the pathway in horses, more input has not been shown to overcome it.

The alternative is to skip the question altogether by providing EPA and DHA directly, at which point the conversion step becomes irrelevant because the finished product is what arrives.

That is what algae-derived omega-3 does, and once EPA and DHA are supplied directly the question changes: not whether the conversion is working, but whether the dose is enough and consistent enough to matter.