Ketones, Butter, and Niacin
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wabmester
Posts: 2,748 Member
Late night reading:
Anti-inflammatory effects of the hydroxycarboxylic acid receptor 2 (PDF)
Backstory: I went low-carb to reduce TG and increase HDL. Before I tried low-carb, I tried Niacin (Vit B3). It worked pretty well -- reduced TG and increased HDL, but it had a couple side-effects: flushing and increased fasting blood glucose. So I discontinued use.
The paper above describes a receptor -- HCA2 -- that is present on fat cells (and others). It basically turns off the fat cell.
The ligands for the receptor are BOHB (ketones), butyric acid (in butter), and niacin.
The receptors are also present in keratinocytes -- skin cells. And that's involved in the niacin flush reaction.
Some people report a flush reaction on low carb. Since BOHB is a ligand, it could be that the flush is a side-effect of high levels of ketones in the blood. The levels of butyric acid in butter are probably too low to cause the flush.
Why would ketones turn off fat cells? To prevent ketoacidosis. It's a negative feedback signal letting the body know that there's enough circulating fat.
Might be one of the mechanisms by which niacin reduces circulating TG, too.
Oh, I almost forgot the best part. This action by these three ligands to turn off fat cells is VERY anti-inflammatory. Which might explain why my CRP was close to zero.
Who knew these three completely different compounds might achieve some of the same benefits through a shared mechanism? Exciting stuff.
Inflammation is associated with a number of diseases processes,
including atherosclerosis, obesity, diabetes, multiple sclerosis
and cancer. There is mounting evidence summarized in this
review that the G-protein coupled receptor HCA2 plays an
important role in modulating inflammation in multiple tissues
and clinical situations (Table 1). Ligands for the HCA2 receptor,
including niacin, MMF, β-OHB and butyrate activate the
receptor, resulting in a variety of inflammation-modulating
signaling events.
Anti-inflammatory effects of the hydroxycarboxylic acid receptor 2 (PDF)
Backstory: I went low-carb to reduce TG and increase HDL. Before I tried low-carb, I tried Niacin (Vit B3). It worked pretty well -- reduced TG and increased HDL, but it had a couple side-effects: flushing and increased fasting blood glucose. So I discontinued use.
The paper above describes a receptor -- HCA2 -- that is present on fat cells (and others). It basically turns off the fat cell.
The ligands for the receptor are BOHB (ketones), butyric acid (in butter), and niacin.
The receptors are also present in keratinocytes -- skin cells. And that's involved in the niacin flush reaction.
Some people report a flush reaction on low carb. Since BOHB is a ligand, it could be that the flush is a side-effect of high levels of ketones in the blood. The levels of butyric acid in butter are probably too low to cause the flush.
Why would ketones turn off fat cells? To prevent ketoacidosis. It's a negative feedback signal letting the body know that there's enough circulating fat.
Might be one of the mechanisms by which niacin reduces circulating TG, too.
Oh, I almost forgot the best part. This action by these three ligands to turn off fat cells is VERY anti-inflammatory. Which might explain why my CRP was close to zero.
Who knew these three completely different compounds might achieve some of the same benefits through a shared mechanism? Exciting stuff.
Inflammation is associated with a number of diseases processes,
including atherosclerosis, obesity, diabetes, multiple sclerosis
and cancer. There is mounting evidence summarized in this
review that the G-protein coupled receptor HCA2 plays an
important role in modulating inflammation in multiple tissues
and clinical situations (Table 1). Ligands for the HCA2 receptor,
including niacin, MMF, β-OHB and butyrate activate the
receptor, resulting in a variety of inflammation-modulating
signaling events.
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Replies
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Ooh interesting, I've definitely experienced a very painful flush. And my rosacea has been absolutely awful, worse than ever before in my life. I've been at a loss because I've researched it and everyone else seems to be reporting a decrease in rosacea.
All of my other inflammatory issues seem to have improved. All I could think is that it's a gut microbe issue throwing off the bacteria in my skin. But now I'm wondering if it's tied to the flushing issue? I had kind of been lumping the symptoms (flushing, rosacea) together, not sure which was causing the other.
Excited to hear about your CRP @wabmester can't wait to see if my results have changed.0 -
Cool! Explains some of my early symptoms while adjusting! Thanks Wab!0
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I take no flush niacin and it works okay. No noticeable increase in heat or flushing. I do have roseaca so my cheeks are always reddish though.
I read someone around here was cutting back on coconut oil because of the histamine reaction to it which worsened their roseaca. Who was that.... Anyway, could that be part of increased flushing?
Congrats on the low CRP @wabmester !0 -
What I got outta this is eat more butter.0
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Ya know, I'm pretty tired of MFP deleting half what I type...
I was being funny. Just imagine I was being funny...0 -
I don't think coconut oil has any butyric acid -- it's a short-chain (4C) SFA that's a fermentation product. Our gut bacteria make some. And cows make a lot.
http://wholehealthsource.blogspot.com/2009/12/butyric-acid-ancient-controller-of.html
Coconut oil does have a thermogenic effect due to the MCT, though. The added heat could also cause a flush reaction.
And, yeah, I think I'm going to eat more butter too. 0 -
I had a handy chart with all the fatty acids in all kinds of fats. Butyric wasn't listed for coconut oil. I'll see if I can find that link.
Ok. Here ya go.
http://www.chempro.in/fattyacid.htm0
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