How much DHA (docosahexaenoic acid, a long-chain omega-3 fatty acid) does the human body make? It depends. It’s not correct to claim a flat rate, say 1% or 10% or 15% of short-chain omega-3 gets converted to longer chain omega-3s like DHA. Each person is different. Even within a person, that rate changes. One variable that affects the rate is how much fat we eat.
This next study compared the effect of a low-fat diet (20% energy) to a high-fat diet (45% energy) on type of fats in the blood. The diets had the same calories and the same proportions of fatty acids (1:1:1 for poly:mono:sat). Designing these diets was a challenge.
Total Fat Intake Modifies Plasma Fatty Acid Composition in Humans, The Journal of Nutrition, February 2001
It was a crossover design, so participants ate one diet for a month, then their usual diet for a month as a wash-out, then the other diet for a month.
When they ate the low-fat diet, they had higher levels of omega-3 (n-3) fatty acids and lower levels of omega-6 fatty acids in their blood compared to the high-fat diet. Specifically, for example, compared to eating a high-fat diet, eating a low fat diet resulted in almost 30% more DHA in phospholipid fatty acids and 36% more DHA in cholesteryl esters.
The low fat diet was associated with significantly greater total (n-3) fatty acids, 20:5(n-3) and 22:6(n-3) levels in plasma phospholipid fatty acids and cholesteryl esters.
Eicosapentaenoic acid or EPA is 20:5(n-3) and docosahexaenoic acid or DHA is 22:6(n-3).
The consumption of a low fat diet promotes an increase in the level of total and highly unsaturated long-chain (n-3) fatty acids (>C20) and a decrease in the total (n-6) content of plasma phospholipid and cholesteryl ester fatty acids. The observed modifications in phospholipid and cholesteryl ester fatty acids in response to a low fat diet are similar to those observed when (n-3) fatty acids of plant or animal origin are fed. This may explain some of the beneficial effects of low fat diets.
How can you end up with higher amounts of EPA and DHA, if you’re not actually eating them?
This change is likely related to decreased competition for the enzymes of elongation and desaturation, with reduced total intake of 18:2(n-6) favoring elongation and desaturation of available (n-3) fatty acids.
What I didn’t realize about this study the first time I read it was that the high-fat group consumed MORE PREFORMED DHA than the low-fat group. They ate more fish. But they ended up with LESS DHA in blood.
Recall that this was a crossover design. So the same person’s conversion rate changed depending on how much fat they ate. You can’t just say 1% or 15% conversion; the background diet matters.
It doesn’t make sense to me that we would need to supplement with something the body produces, unless we are somehow thwarting that production.
The paper above was in 2001. Here’s a more recent review that continues to say:
In conclusion, while the current data support the suggestion that n-3 LCPUFA status in humans can be increased in the absence of increased n-3 LCPUFA intake, there is a need for well-controlled and adequately powered studies in males and females in order to evaluate whether these diets could be a viable alternative to n-3 LCPUFA supplementation for achieving improvements in human health.
– The effect of modifying dietary LA and ALA intakes on omega-3 long chain polyunsaturated fatty acid (n-3 LCPUFA) status in human adults: A systematic review and commentary, Prostaglandins, Leukotrienes and Essential Fatty Acids, April 2015
The study at the top was small (although well-controlled: food was provided, dinners served in metabolic ward, it was cross-over with wash-out periods) and it mixed men and women of a broad age range (22 to 65 years old). There was 100% retention, everyone finished the study. To scale this up would be an enormous expense – an investment, I imagine, that would not be returned since the intervention requires doing less of something: eating less fat, especially the type (omega-6) that our diets are flush with from all the subsidized corn and soy oils we eat. If it’s not a pill, drug companies won’t pay for it, and drug companies pretty much own academic and government research these days. The agricultural industry, producers of all our omega-6, would likely also discourage it.
Let’s look at a 10% conversion rate…
There are about 3 grams of ALA in 7 walnut halves and 1 tablespoon of ground flax seeds. If our livers converted 10% of that 3 grams to DHA (assuming a whole lot of things but this is hypothetical), that’s 300 mg. And most plant foods contain ALA so it’s likely we get more than 3 grams a day. That 300 mg DHA is more than the 250 mg Dr. Greger advises taking in an expensive, partly-oxidized, ultra-processed, algal-derived omega-3 pill.
There’s also this:
“The best conversion rates [of ALA to EPA and DHA] are by individuals that don’t consume DHA and EPA.”
Omega-3: ALA intakes enough for EPA/DHA levels for non-fish eaters?
I’m happy to see there’s something people can do besides taking a pill: Eat a low-fat diet.