This is part of a three part series:
So I have a fancy metabolic tester to track my metabolic rate. It’s honestly pretty amazing if you have $7500 burning a hole on your pocket. Sometimes they have deals and I’m an affiliate so if you give them my code “BMarsh”, you’ll get $600 off.
If you can’t afford a metabolic tester, here’s a great idea from the r/SaturatedFat reddit board where ideas around The Croissant Diet are discussed. See how long you can hold your breath. Figure out what your baseline is, repeat it a few times, do your dietary change or whatever, then see how your time changes.
I’ve worked out a testing protocol that works for me. When I wake up I’m frenetic. I pace and think. That’s my happy place. I usually drink a pot of coffee while I do this. Yes, I said a pot. A french press really, but a good sized one. At that point I’ve burned off my morning pacing energy and I sit down with the metabolic tester right around 10am. The first five minutes of the test while I sit on the couch don’t count. That’s my settling in time and things are changing on the meter. Five minutes in the numbers tend to plateau. I take a five minute reading, then I get up and pace, which is my natural state as I’ve mentioned. My pacing happens at a pretty steady 2.7 MPH. That’s my protocol, it works for my. It’s not really a true “Resting Metabolic Rate” because I already had a pot of coffee and spent three hours pacing, but it’s internally consistent, which is the important thing for this.
I did the Feasting Mimicking Diet in the summer of 2020 and received the device in the middle of that trial. After the FeMD, I went back to “normo” eating because I wanted to get a true baseline for myself. I was very busy at the time, so this was easy. “Normo” eating is typically two meals a day, something like eggs and toast with butter late morning followed by steak and potato in the evening. I wasn’t doing any stearic acid supplementing (or any other supplementing) because I wanted to get my baseline.
Metabolic testers give you a bunch of data but the most important one by far is how much Oxygen you are consuming, defined as volume of Oxygen per minute measured in CCs. By mid-October, my Oxygen consumption (VO2) was typically in the high 200s. This is honestly not great for someone my size, even though I’m quite muscular. 280 CC’s VO2 is my torpor number. My pacing number was around 760. Metabolic testers also give you CO2 released, which in theory can tell you if you’re burning fat or carbs, but my VCO2 numbers are wonky. It’s not the device, it’s a me problem. I’ll have more to say about this later.
Over the next 8 weeks I consumed one teaspoon per day of sterculia oil. This is probably too much, it caused me some inflammation, but it DID have a notable increase in my metabolic rate, showing a steady increase the first week before plateauing in the mid 300’s with the pacing number averaging around 850. Not bad!
Eating Fat Bomb Fries, Getting Hyper
Mice who lack SCD1 have very high levels of VO2, fail to store fat and are called “hypermetabolic”. On January 2nd I took my first crack at hypermetabolism. I had been taking hi-dose sterculia oil for two months before stopping on December 15th to complete my safety/half-life trial. My blood test from January 5th showed that at that point the stearic acid in my red blood cell phospholipids was all the way up to 25% after being under 11% in October before I started the oil. I hoped this was reflected in my fat tissue.
Now it was time to combine the effects of the sterculia oil, with my most devious metabolism increasing diet: the Feasting Mimicking Diet. I already knew that my metabolic rate was higher during the feasting mimicking diet than it was after my “normo” diet. In August during FeMD my typical numbers were around 360 Resting and 900 pacing, not dissimilar to what they were with just hi-dose sterculia oil. So what if I combined them?
The reasoning is pretty straight-forward if you’ve followed this blog. The large amount of dietary stearic acid causes mitochondrial fusion and increases the rate of fat burning. My stored fat is hopefully now more saturated so that the blend of fat entering the mitochondria is highly saturated. This should drive ROS, production, mitochondrial uncoupling and therefore metabolic rate. I did my first feast of Fat Bomb Fries and Pancake Chicken the evening of January second then didn’t consume solid food again until my second feast the evening of January 4th. Look at what happened.
|VO2 Resting||Heart Rate Resting||VO2 Walking||Heart Rate Walking|
|Beginning of Sterculia Oil.|
|End of Sterculia Oil.|
|Beginning of Feast/Fast Stearic Acid Macro Dosing.|
|Red blood cell membrane stearic acid phospholipid level at 25%.|
On the third, I got one of my highest readings to date, which was surpassed on the fourth. After the second feast meal, on the morning of the fifth, i recorded my highest ever Resting reading – 416! For the second straight day I recorded a pacing VO2 of over 1000 – a nice round number! The numbers declined over the rest of the month in parallel with my stearic acid numbers….
I consider this experiment to be a proof of concept. Something happened. I saw a response. That’s cool. Now we have to figure out how to harness the power for long term gain.
8 thoughts on “Sterculia Oil: Metabolic Results Number One”
Did you take your basal temp?
It would be nice if you took and reported your breath holding durations. I for one would like to see the magnitude changes and correlation with your other measures.
Honestly, I’ve never actually done this, but I think it’s a good idea. I CAN say that I’ve been supplementing with a lot of searic acid the past two days. O2 consumption is up ~15% on my PNOE device (from ~330 to ~ 380). I normally gulp a pint of water in the morning, but this morning I had to stop multiple times to breathe.
How do we know that fused mitochondria is fat-burning mode?
To quote from the paper:
“We previously reported that reduced C18:0 levels lead to reduced mitochondrial respiration in Drosophila16, possibly due to reduced mitochondrial fatty acid beta-oxidation. To test if beta-oxidation is affected, we measured long chain acylcarnitine levels in the blood samples. Acylcarnitines are fatty acids coupled to carnitine that are ready for mitochondrial import for beta-oxidation. When beta-oxidation is impaired relative to the fatty acid supply, these long chain acylcarnitines accumulate and are released into the blood where they can be detected, forming the basis for screenings of newborn babies for beta-oxidation defects. . Interestingly, we found that serum long chain acylcarnitine levels increase significantly after a 2-day low-fat vegan diet (“0 h” vs “basal”, Fig. 3a, b). Conversely, long chain acylcarnitine levels dropped significantly after ingesting the C18:0 drink but not the mock drink (Fig. 3a, b), suggesting that C18:0 intake increases fatty acid beta-oxidation in vivo. Particularly striking, C18:0 ingestion leads to an increase in circulating C18:0-TAG levels (Fig. 2), but causes a decrease in circulating C18:0 acylcarnitine levels (Fig. 3a), indicating that the acylcarnitine drop is not due to reduced substrate availability but rather to increased acylcarnitine usage. “
Do you have black coffee when fasting or other stuff added too?
Black coffee or sure. I can’t even live without black coffee. Also red wine.
Has anyone noticed a change in bowel habits usung sterculic acid?
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