Post-rice OmegaQuant: 8% linoleic acid

An interesting exercise in understanding the OmegaQuant Complete test

This post is super technical about OmegaQuant Complete tests and fatty acid synthesis. If that’s not your cup of coffee, maybe just scroll and look at all the colorful pictures and graphs I made.

Why was this OmegaQuant Complete different?

My recent rice diet experiment was testing 3 things:

• Would I lose fat? (No)

• Would my Non-24 come back? (No)

• Would it lower my linoleic acid stores more rapidly? (Maybe)

The Non-24 part was pretty obvious after a week. After 2 weeks of my sleep staying normal, I was 100% certain.

The fat loss part took a bit longer, but the scale did not go down. Instead, it went up. A DEXA revealed that I had gained a little bit of lean mass, but more fat. So the feedback there was clear after a month.

But what about the linoleic acid?

Why would a HCLFLP diet deplete linoleic acid faster?

There is a hypothesis floating around r/SaturatedFat that very-low-fat diets like the potato diet, Kempner-style rice diet, and similar diets are particularly effective at depleting linoleic acid in adipose tissue.

There are some mechanistic reasons for this that seem to make sense, and a few anecdotes. Members of that subreddit who have depleted their linoleic acid rapidly tend to have done either a lot of fasting, or substantial stints on a HCLFLP diet, or both.

One mechanistic reason is simple: if you don’t eat any fat, your body has to use the fat in your adipose tissues or make its own. Since linoleic acid is (conditionally) essential, meaning the body cannot make it, this would force the body to use up more of it than if you were eating fat.

Even if you ate a low-LA diet like ex150, it would still contain about 2-3% linoleic acid, which is likely more than the “essential” component the body requires on a day-to-day basis.

Think about it this way: your bathtub leaks 2% water every day (essential fatty acids), and you pour in 2-3% every day. Even if 2-3% is a very low number compared to the overall size of your bathtub, it’s more than enough to cover the drainage.

If you stopped pouring in water altogether, the level in your tub would suddenly start going down much faster.

Of course this analogy is leakier than the bathtub in it, but I hope you get the point.

Depleting LA at 2% with 0% intake is likely a lot faster than at 2% with 2-3% intake, because 2-3% is a small percentage, but it is 100-150% of 2%, a very big percentage.

Anyway, that’s the hypothesis.

But linoleic acid is difficult to test. Since we can’t directly test our adipose tissue (and believe me, I’ve looked), the best proxy I’ve found so far is the OmegaQuant Complete test.

OmegaQuant Complete pros/cons

The OmegaQuant Complete (OQC) has a few upsides:

• No prescription needed

• Only $100

• Available on Amazon.com

• Can be done at home

• Only a finger prick blood test

But it also has a massive downside:

• The linoleic acid number on the OQC is only a proxy for adipose linoleic acid, and there are quite a few confounders and contextual factors

I’d liken the OQC to a cheap compass. It might generally point in the right direction, but you need to hold it steady, you need to ensure there’s no magnets nearby, and you need to know about the magnetic vs. geographic north pole.

But if that’s all you got, that’s all you got, and you better learn to use it correctly.

This post is mostly about these confounders and contexts, and how to interpret the OQC. This might seem a bit like reading tea leaves, and it is. Yet I don’t know of a better way to estimate our adipose linoleic acid % so far, and I think it’s a decent enough proxy that I’m sticking with it for now.

I’ve previously written about interpreting OmegaQuant Complete results.

ZOMG 8% is super low!

8% linoleic acid shocked me. That’s -9% vs. last month and by far the lowest I’ve ever tested.

It is the 5th lowest data point in the database:

Look at my all-time OQC graph:

Oh wow! Did the rice diet instantly teleport me into the end zone of PUFA depletion? I’d never even seen the yellow zone, and now I was deep into the green!

To make this clear up front, no, I don’t think so. This result merely shows us an interesting quirk in our fatty acid metabolism, one that I’d picked up on earlier, when comparing various long-term PUFA depleted people and their OQCs. This time, I hit it myself.

Back then, I called it the “5% vs. 10%ers: two types of LA-depleters”.

To briefly summarize: even some people who had strictly avoided PUFAs from all sources but beef for 8-9 years “only” tested at ~10.5% LA on the OQC.

Yet some people went dramatically below that, testing as low as 4.97%.

My intuition, and the rest of the fatty acid profile provided by the OQC, made me think these people didn’t actually have dramatically lower adipose LA, they merely had upregulated fatty acid synthesis.

Our body can generate many fatty acids that it requires, basically all of them besides the “essential” ones. That’s the definition of “essential” in nutrition - we can’t make it ourselves.

What I’d noticed was that the “sub-10%” depleters had much higher MUFA than the 10.5%ers or “normal” (=not depleted) people.

This told me that the sub-10%ers probably had a similar level of adipose LA as the 10.5%ers, but their bodies were producing much more endogenous MUFAs and possibly SFAs via DNL (de novo lipogenesis).

A common thread among the sub-10%ers: they ate very low to near-zero fat diets, or they were extremely lean, or both.

Both of these would induce the body to produce more fats via DNL. When will the body produce more of its own fat? When you don’t eat enough, or you don’t have enough available from your own body fat stores, or both.

In short, that’s what I think happened to me on the near-zero-fat rice diet.

Rice diet make DNL go brrrrr

Walter Kempner, gleefully operating the fatty acid printer

My rice diet was approximately fat-free. White rice contains just about 0% fat, as does fat-free (duh) marinara sauce.

That might not be very healthy or sustainably long-term, but it was sort of the point of this linoleic acid depletion experiment. And I was only doing it for a month.

Let’s look at the entire fatty acid profile on my OQC:

Sure, LA is down to 8%. But Palmitic is up 5%, Oleic is up 8%, and Palmitoleic is up 3.5%. Interestingly, Stearic (SFA) and Arachidonic (the actually-essential omega-3 PUFA) are both down a bit.

Let’s visualize it for easier comprehension:

These aren’t all the FAs on the OQC, but it’s all the major ones making up more than 2%. We see the massive Linoleic drop, but we also see Arachidonic and Stearic drop a bit. But Palmitic (SFA), Oleic (MUFA), and Palmitoleic (MUFA) go up dramatically.

Here’s another graph that’s just split up by PUFA/MUFA/SFA:

In short, PUFA went way down, MUFA went way up, and SFA stayed pretty flat, at least in the overall historic context. Maybe it went up a tiny bit, but it might well have been noise. Apparently, Stearic went down by almost as much as Palmitic went up.

Luckily, I’d been tracking all those fatty acid enzyme markers that Brad at Fire in a Bottle had been talking about. I have a little calculator & explainer blurbs here.

There are various enzymes in our bodies that can elongate (add carbons to a fatty acid) and desaturate (turn SFAs into MUFAs) the fatty acids in our bodies. We (along with all mammals, I think) lost the ability to desaturate MUFAs further into (omega-3/6) PUFAs, which makes these PUFAs somewhat essential to us. C. elegans worms have this ability, and scientists are doing fucked up stuff by implanting these genes into mice.

In any case, there are various steps in this whole fatty acid synthesis business and I found this picture online that explains the various players pretty well:

Stolen from http://srebp1a.com/future-research/

You can see that the body initially produces only palmitic acid (C16:0). This is then elongated to stearic acid (C18:0) or desaturated into palmitoleic acid (C16:1). The stearic acid, in turn, is desaturated into oleic acid (C18:1), and palmitoleic can be elongated to oleic acid as well.

This could explain why my stearic acid went down: since it’s sitting between palmitic and oleic, it might be very high flux, but the level at any given time might not have been very high because it was so in demand.

But why did palmitoleic, the other “in between” step, go way up then?

Who knows. Systems theory! Ugh!

Anyway.

We can estimate the activity of these enzymes by calculating various ratios between 2 fatty acids: the one that a given enzyme is consuming, and the one it is making. Again, the ratios are explained here.

Now let’s graph some of them:

You can see that all of them spiked dramatically. D6D is over 7x of my “normal” level, whereas SCD1/DNL went up 1.5-2x.

For the record, D5D did not go up, it went down if anything. D5D is the last step involved in making Linoleic Acid into Arachidonic Acid, so maybe I didn’t have enough Linoleic Acid to keep that up? From an average of about 9.0 down to 6.7, that’s a drop of about 25%.

Mead Acid - the real MVP?

One topic that I’ve almost never seen discussed except by the excellent people of r/SaturatedFat is Mead Acid. Mead Acid is an omega-9 PUFA that the body can produce endogenously from Oleic Acid.

Its presence is an indicator of “essential fatty acid deficiency” and it’s speculated that Mead Acid can (partly?) help fill that role as it’s also a PUFA, although a 20-carbon one, whereas the essential ones are 18-carbon.

(It’s named after the guy who discovered it, not the historic beverage.)

Unfortunately, the OQC does not test for Mead Acid.

If I were a betting man, I’d wager that my Mead Acid was significantly up this time vs. my previous tests, possibly the main reason for elevated Oleic Acid.

But we don’t know since we can’t test it.

tl;dr: my adipose linoleic acid almost certainly didn’t really decrease by 9%

What this shows us is the weakness or technicality in using the “cheap compass” from the earlier analogy.

When eating a near-zero-fat diet, we’re in effect operating in a zone where the magnetic vs. geographic north starts making a difference. For most people, these will be the same in a practical sense. But if you’re trying to reach the North Pole with a sled and some dogs, you better know the difference.

That’s what we’re doing here.

Now, did my adipose linoleic acid actually go down by a significant amount? I think that this test can’t tell us that. I’ll have to re-test after a month or so of eating my normal high-fat cream diet again.

If the DNL numbers are back in familiar territory, but my LA% is down to a new low, then I’d call that evidence of success.

Remember, the “good” and “bad” zones are relatively close:

Before the rice diet, I’d never tested below 15% LA, and never below 16% fasted. The 1% difference could’ve been from my copious cream intake when I was still taking non-fasted OQCs.

If I test 14% or even 15% fasted next time, just a 1-2% reduction from my usual 16% result, I’d consider that a HUGE success. A single month of Kempnering is quite tolerable. If it depletes significantly more PUFAs than many months of a low-PUFA but high-total-fat diet like ex150, it might be very worth our while.

Can we normalize for fatty acid synthesis?

Ever since I ran into the 5% vs. 10% PUFA depleters, I had been thinking: can we find one unifying factor that lets us compare all of them on a level playing field?

Can we normalize for fatty acid synthesis? I didn’t want to use DNL (the ratio) per se, because that’s partly defined by linoleic acid - obviously, it would go up if linoleic acid went down.

But what if we normalized it by the fatty acids involved in fatty acid synthesis?

LA/(1-OL-PA-POL)

It’s quite a mouthful. I don’t have a name for it. Maybe “FASNLA” (Fatty Acid Synthesis Normalized Linoleic Acid)? Or “LAOLPAPOL?”

Maybe not.

Catchy name not withstanding: this is linoleic acid divided by 100% minus the sum of oleic acid, palmitic acid, and palmitoleic acid. I suppose I could throw stearic in there as well, not sure. For now, let’s just do these, as stearic seems inversely related to fatty acid synthesis, at least in me, this one time.

What this means, in essence: the higher your fatty acid synthesis,
the lower we’d expect your linoleic acid to be.

As your FAS (fatty acid synthesis) markers go up, the denominator (number we divide by) decreases, and the total fraction thereby increases. People who have very high FAS get “punished” a little in their LA number, as it looks artificially high.

Of course, all of this is pretty rough and guesstimated, but let’s give it a shot.

Let’s look at our all-time champions, the long-time PUFA depleters:

Name              LA     LA-normalized   Comment

Mr. X             10.57  0.19            9 years no PUFA
Infamous_Article  10.55  0.18            8 years no PUFA
Yvonne            10.21  0.17            4 years no PUFA, Peating
Health-consultant 5.42   0.17            OJ, milk, honey diet, lean
Omshivji_1        4.97   0.13            Lean, fruit, skim milk
Omshivji_2        7.6    0.21            Lean, fruit, skim milk
M                 6.43   0.14            Keto AF, lean
Sudas             13.18  0.30            Keto AF
Coconut_3yr       12.06  0.27            3+ years no PUFA, low-fat/fasts

(I am once again begging Substack to add tables so I don’t have to spend half an hour hammering space and aligning these manually.)

Lo and behold, a lot of them are really close together! Especially the really-long-term avoiders. We can see that the <10% people (Health-consultant, Omshivji, and M) aren’t that far off from the 10%ers like Mr. X, Infamous_Article, and Yvonne.

r/SaturatedFat’s own user WhatsUpCoconut, who has been aggressively depleting PUFAs, dishing out advice on the subreddit, fasting, and eating HCLFLP, is just over 12% and thereby quite close.

Sudas, a 3-year Keto AF (animal fats) carnivore who mainly eats fatty beef, is at a very respectable 13%, and a little bit behind in terms of normalized LA.

(Interestingly, the people on this list who eat a really low-fat diet also have higher Palmitoleic Acid, like me on the rice diet. Maybe Palmitoleic is just a really good sign of fatty acid synthesis happening.)

What’s different between Omshivji’s first & second test? I’m not sure. The only real difference I see is that his linoleic & palmitic acid both went up about the same (2.5-3% each). Maybe it’s just noise at that level, since the fatty acid profile is much more influenced by your day-to-day diet & fatty acid synthesis than adipose levels.

What about M? Her test is unique in the ones I have: she has very high fatty acid synthesis, but she has higher Stearic Acid, not Palmitoleic Acid.

The reason could be that her fatty acid synthesis is caused not by super-low fat intake (she’s a keto AF/carnivore eater, after all), but by very low body fat levels. All the other high-FASers we have eat a low-fat to super-low-fat diet.

Maybe this explains the different pathways that fatty acid synthesis can take to arrive at making Oleic Acid: low-fat eaters have higher Palmitoleic Acid levels, lean high-fat eaters have higher Stearic Acid levels? Something curious to look out for in future results.

What does normalized LA say about my Rice Diet?

Not bad! The overall curve looks very similar to my LA curve, with the peaks slightly offset. But that massive drop at the end, after the rice experiment, is still there, despite normalizing for all the fatty acid synthesis markers.

I.. think that’s a pretty good sign my LA actually went down a bit?

If we now reverse the normalization, but plug in my previous tests numbers for fatty acid synthesis, we arrive at: 12.05%. Dropping 4% in one month would be glorious.

Of course it could just jump back up. Maybe my normalization method is trash. Maybe it’s not enough to counter the temporary tea-leaf effects of the OmegaQuant Complete. Maybe I’m seeing patterns where there are none.

We’re now ready to test 2 hypotheses:

1. It would be pretty cool to have a somewhat accurate, normalized number for PUFA depletion that unifies fatty acid synthesizers and others

2. It would be pretty cool if you could massively deplete your adipose LA just by Kempnering for a month here or there

Time will tell. I’m excited for the next OmegaQuant.