Thursday, October 04, 2007

Niacin and beta hydroxybutyrate

There is nothing about antioxidants in general that affect lipoprotein levels. Niacin undoubtedly does have significant action on blood lipids so undoubtedly is more than an antioxidant. I find that interesting. Why should that be? Many biological processes act through receptors. The niacin effect on lipids, and the niacin flush (ever tried this? It's fun fun fun, not!), are receptor mediated. Clever people have found at least a couple of receptors. The first was HM74, now joined by HM74A. These receptors were not sitting there waiting for either psychiatrists or cardiologists to prescribe multigram doses of nicain, useful though that may be.

No, they have a natural ligand, beta hydroxybutyrate. Beta hydroxybutyrate is a substance dear to my heart, and your heart too, see here. It's a ketone body, naturally manufactured by the liver in times of starvation or carbohydrate restriction. Plus times of coconut fat consumption too, as medium chain triglycerides (MCTs) will produce ketone bodies even in the presence of carbohydrate. By the way, this is not my preferred fat, and it worries me a little that humans break down MCTs as fast as the liver can do so, plus they are shunted down the hepatic vein rather than the thoracic duct, minimising their access to the general circulation. It just reminds me of our metabolism's approach to fructose a bit. Still, coconuts have an excellent track record as a human food in the tropics, so I'm probably just being a bit paranoid here.

Low carbohydrate diets naturally produce ketone bodies. They will certainly elevate HDL cholesterol levels too. To which you may ask, "so what?". Well, elevated HDL cholesterol appears to be a marker of a high fat, low carbohydrate diet and its associated beta hydroxybutyrate. So it is a marker of good things happening in the metabolism. As such I welcome it, but not if it is an effect of some drug. Of course if your primary protection against heart disease is normal blood sugars and low insulin levels the elevated HDL-C is not essential, as seen on Kitava. On western food supply a little exercise plus LC eating seems to be the easiest way to maintain normal blood sugars, and coincidentally elevated beta hydroxybutyrate and so HDL-C. Statins and niacin may elevate HDL cholesterol but my guess is that their benefits (however small from the statins) are unrelated to their effect on HDL-C. And of course, once you are on a drug to elevate HDL-C, there is no way of telling if your metabolism is doing well or badly in terms of insulin sensitivity. If you combine a statin plus niacin plus the dreaded AHA Coco Krispies based low fat diet, you may well be on the road to a cardiovascular disaster, despite having the appearence of a "good" "good" cholesterol level...

Peter

8 comments:

mtflight said...

if MCT oil (a large component of coconut oil) raises triglycerides... does this form of dietary triglyceride have any influence on LDL particle size (changing subclass pattern A to B, as observed by Krauss et al.)


I would think small dense LDL particles (the atherogenic subclass pattern B), are the result of high triglyceride PRODUCTION in the liver not of free triglycerides in the blood.

Peter said...

Hi mtflight,

As I understood it MCT are hydrolysed in the intestinal wall to free fatty acids which then enter the portal vein for a direct trip to the liver. In the liver they are rapidly oxidised and/or converted to ketone bodies. They don't seem to get in to chylomicrons much and, although they don't seem to raise VLDL particle numbers, I've not seen any information as to their effect on LDL particle subtype. They can't be worse than cornflakes and skim milk, probably a lot better!

Peter

mtflight said...
This comment has been removed by the author.
mtflight said...

Thank you Peter.

On April 2007 I, went to strict low carb because my cholesterol was slightly elevated (nothing really as you can see from the chart linked below). As expected it dropped by June 2007.

Starting June, I cut-out omega-6 PUFAs from veggie oils/fried things, and started using coconut oil and taking fish oil capsules regularly (also started taking vitamin D, about 4000IUs/day). I would make a smoothie with vanilla flavored protein, coconut oil, heavy cream and orange flavored sugar-free psyllum husk in the morning, eat hamburgers without the bun etc for lunch/dinner.

Unfortunately I take a thyroid supplement and it was being malabsorbed thanks to the smoothie. The cholesterol readings went through the roof. At the same time I had been doing Intermittent Fasting as well.

I corrected the smoothie in the morning and my TSH (thyroid stimulating hormone levels) became normal as of October 07, but the lipid anomalies continued.

Low thyroid hormone wipes out the LDL receptors, but I assume they come back when the normal levels are restored.

Here is a link showing the basic lipid parameters as well as TSH and Thyroid dosageThe Feb 14 08 is a direct-LDL measurement (what a waste of money).

I am thinking the coconut oil explains the triglycerides over 100 on the low-carb diet (otherwise almost unheard of, at least in my experience).

The higher saturated fat content could account for the higher LDL, but I suspect it was a combination of saturated fat and coconut oil.

Starting in January I started taking niacin in large regular dosages, as an alternative to a statin (Doctor asked me what I wanted to do, but insisted we adress the LDL).

I discontinued coconut oil this week, and will retest my cholesterol in a month or so.

mtflight said...

June update:

Had a Lipoprofile NMR

TG 69
TC 256
HDL 41
LDL 201

Tot-Cholesterol down 15 pts (from Feb 14).
LDL-C, down 14 pts
HDL-C, down 1 pt,
Triglycerides, down 26 pts (no longer consuming coconut oil)

Very high LDL-P particle count(2576) and very high Small LDL-P particle count (1687)

LDL-P diameter is barely pattern A (20.8 nm), but that's the big pattern which is good.
L HDL-P 5.9
L VLDL 0.6
Fasting insulin 5.2 (this seems good, no?)

I continued high fat low carb, mostly saturated, very little added monounsaturated.

I'm kind of puzzled as to why particle diameter is "barely" Pattern A (I believe 20.5 and below is Pattern B)

Also all the flags on the high particle counts are not pleasing. Am I requesting the best of both worlds?

Do we high fat, low carb eaters have high particle counts? I thought the hypothesis is that consuming a lot of saturated fat, causes the LDL to have more cholesterol in it, thereby less, but larger particles.

Thanks for speculation. Considering niacin again, to see if that changes particle counts, and pushes the L LDL-P diameter further into the large pattern.

Peter said...

Hi mtflight,

This is too interesting for a one line reply! It's not being ignored, just slotting it in to previous posts. I was going to put up a post on oxLDL and glycated LDL and the relevance of lipid parameters. It's just unfortunate that I'm back in full time work and the work keeps getting in the way of everything!

Peter

mtflight said...

Thanks Peter! I look forward to your posts. If possible let me know on here when u post them so that I don't miss them.

Regards,

Alex

gunther gatherer said...

mtflight, I just took the same step as you, and took out coconut oil as well as butter and cream (all high MCT containing), and found renewed weight loss where I had stalled as well as other benefits, such as better sleep. In my case, I consider deeper and more restful sleep to be a signal of lower insulin levels. I could never have that when eating my 5 fruits a day...

I'm not a scientist, but I am a keen observer and I'm starting to feel that what Peter says is true, the body dumps MCTs fast because it doesn't want it around, like alcohol or PUFAs.

I'd be interested to know if you experimented with both removing coconut oil AND dairy fats, switching to mostly beef drippings and lard. Betcha you'd see positive changes in your trigs...

To your health,
G