Quick Fat Facts
August 28, 2011
A few months ago, I was pointed to primalmeded – a burgeoning blog in this here paleosphere.
Regretfully, I just added her to my rss reader and let the posts pile up (oops). Well I just got around to reading some of her stuff today, and am quite impressed. Ok, that’s enough pumping the tires.
After reading her wonderful two-part series on fat (1, 2), I thought I’d drop by and highlight a few points made.
- We store extra energy as saturated fat (except a relatively small amount of glycogen). If our bodies store it as such, it can’t be unhealthy.
- As we know, MCTs (a saturated fat) provide quick energy. They also promote ketosis, and make up a substantial portion of breastmilk. If evolution points our babies toward ketosis, it’s probably not unhealthy.
- Bacteria in our guts ferment soluble fiber (like that found in apples and berries), yielding Butyric acid (a saturated fat) for our use as energy. If our symbiotic intestinal tenants give us saturated fat (when we eat plant foods that even the USDA calls healthy), it’s probably not unhealthy.
- Plant sources of Omega-3 don’t get the job done. (Chris Kresser has highlighted this in the past.)
- We probably shouldn’t supplement PUFA (even fish oil). Or as she puts it, “Supplementing with artificial sources may just be akin to playing with fire.” [I’ll note that I take Cod Liver Oil – but try to get High-Vitamin or Fermented to maximize micronutrient:PUFA ratio.]
She also details the reasoning behind the oft-stressed recommendation that n3:n6 be consumed in some certain ratio (1:1 or 1:2…etc.).
One more thing to add to our little diagram is the enzymes which actually perform the conversion of short chain PUFA to long chain PUFA. Both families, omega-3 and omega-6, use the same enzymes and therefore they are in competition for them. Too much of the members of one family will interfere with the functioning of the other family. This is where the concept of a healthy 3:6 ratio comes from. High concentration of LA suppresses the conversion of ALA to EPA and DHA. On the other hand too much EPA can cause AA deficiency.
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My questions to you (reader) are as follows:
- If I get EPA, DHA, and AA from diet directly, does the ratio matter at all? (Since I won’t need conversion from short-chain to long, do I need to worry about competition for enzymes?)
- Is this “competition for enzymes” the only reasoning behind this common recommendation? I don’t have the book on hand (on vacation), but I seem to remember something about cell wall stiffness in Protein Power Lifeplan (not that everything in that book is accurate by any means).
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@primalmeded engaged in a bit of tweeting (1, 2, 3) on the subject last night; here’s a summary (paraphrased) of what she had to say:
Ratio of n3:n6 is less relevant if consuming long-chain PUFAs directly, especially while eating grass-fed ruminants. Excess talk about ratio obscures the importance of absolute quantities, i.e. attempting to offset a high n6 intake with high-doses of fish oil daily is the wrong approach. The ratio is somewhat important in terms of membrane stability; Omega-3 are most vulnerable to lipid peroxidation.
Recall that our body’s cells contain fatty acids (as phospholipids) in the cell membranes. Oxidation of these phospholipids is a bad thing.
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