In attempting to figure out how Jack's lipids went awry, I started to focus on the coconut oil that he eats. Normally this wouldn't stand out to me, but consuming it alongside a diet that has 100-150g of carbs per day is somewhat unusual in the paleo world, and what we're looking for are ways in which his diet is veering away from what most do, since most have steadily declining VLDL/TGs/apoB100 that plateaus at a low level.
In this study they managed to triple serum TGs in 6 days with MCT overfeeding. LCT did not produce this effect. They hypothesized that the thermic effect that we all know and love about coconut oil was actually due to the energetically costly process of fatty acid elongation and that a substantial amount of the MCTs were actually being elongated into C16 (palmitic acid) which is our body's go-to fatty acid during de novo lipogenesis. Those palmitic acids would then be esterified into triglycerides and secreted in VLDL.
I'm not sure if this is some part of the reason why the Kitavans have higher TGs than the Swedish or if that's entirely due to their high carbohydrate intake. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.1994.tb00804.x/abstract
Now, for someone doing VLC, this all wouldn't really matter since insulin is kept low, lipolysis and lipid oxidation are not impeded, and appetite is greatly reduced. Muscle mitochondria would readily accept these fatty acids from VLDL and oxidize them for energy. With Jack however it would appear that he has a few pulses of triglyceride synthesis each day coupled with frequent snacking between meals and an elevated insulin level in general. This would greatly reduce TG clearance and you would see fasting TGs rise as they have. 150g of carbs, especially for someone who engages in frequent resistance training should not be enough to cause this, however the manner in which they are eaten could potentiate the TG-increasing effect of the coconut oil. 2 Tbsp a day of coconut oil doesn't sound like a lot but imagine how little of it would have to be circulating in your blood for it to register as elevated TGs.
Luckily, if this is what's happening, there are plenty of possible solutions. He can remove the coconut oil and leave everything as it is and odds are, given that he has a fairly active job, his TGs would gradually drop. What would be better would probably be, whether he replaces coconut oil or not, addressing the failing of his diet with regard to appetite that has caused him to be hungry in between meals and eating all day long. No proper diet should produce that effect. By having big slabs of meat constitute a greater portion of his meals and thus reducing his appetite and eating less frequently while doing more low-intensity exercise in the fasted state, he would rapidly clear the TGs (which also means a reduction in VLDL and apoB100) from his blood, which itself should raise HDL.
The reason why we don't just shrug when we see high VLDL/TGs in spite of what we consider to be a good diet is that they are far more prone to oxidation, consumption by macrophages and conducive to the formation of foam cells and later atherosclerotic plaques than LDL is. It is therefore wise to keep an eye on this parameter and make any necessary changes that would maintain a high VLDL turnover rate in order that there isn't time for oxidation. It seems prudent to also ensure that dietary antioxidants are of sufficient volume to further reduce the chance of VLDL oxidation. HDL would rise as a result because it would no longer be tasked with dealing with oxidized VLDL and would therefore be cleared from circulation at a lower rate.
Now THIS is a hack! This is fascinating Travis. I definitely get my fair share of coconut oil. I always cook my eggs in them, and I always do a 50/50 mix of coconut oil and ghee when cooking tubers. I am totally estimating with that "2 tbsp" by the way. It could be more, but I've never really measured exactly how much I'm using. In fact, now that I think about it, on days that I eat egg and sweet potato together (which is about 2-3 days per week) I take a double portion of coconut oil. We have this tiny ladle spoon that we use for the big nutiva jar. It's about 2 tbsp per "ladle". I will often dump a laddle of that in the pan and cook a sweet potato, and then dump another ladle to cook the eggs in. I think my 2 tbsp of ghee is more accurate, but I'm closer to 4 tbsp of coconut oil in one sitting on many days. I know many people eat that much C/O without even blinking... but in the context of your presentation here, I could see how my C/O consumption, in combination with between meal snacking (even if the snacks are healthy whole foods which they always are), that my liver could continue to push out trigs and VLDL.
I am getting closer to deciding on what my next experimental hack will consist of.
I may be able to whip this deal by making the following changes:
Eliminate coconut oil (maybe not forever, but at least for a specific time frame)
Curb snacking between meals
Workout and walk in a fasted state (including no pre workout drink)
Heavily reduce dairy (specifically butter, cream, cheese)
Eat more of that Slankers GF beef I have just loaded my freezer with
A couple questions come to mind...
Might ghee have the same potential detriment in this equation as coconut oil?
Is it really necessary to reduce my 3 main dairy items above, or is that primarily speculation?
In the context of making the above changes, should I continue to consume starchy carbs (mainly tubers and rice) or should I go LC at the same time?
On another note... that article from Dr Davis today that Meredith references in her comment above has also got my attention. The changes in blood lipids that Dr Davis points out (TGs up, VLDL up, sdLDL up, HDL down) is exactly what happened to me and I did indeed just radically altar my diet and reform my entire body by exchanging fat for muscle in a very whiplash sort of fashion. It could definitely be playing a role here in addition to all the above, especially since many of my other lab results came back strong or at least not alarming in any way.
This is GREAT stuff folks!
My money is on the MCT's obligatory oxidation tamping LCFA oxidation rates down resulting in reduced conversion of VLDL/LDL and/or uptake by adipocytes.
Using radiolabel tracers, Hellerstein's group demonstrated that increased de novo lipogenesis was NOT the source of elevated VLDL in a non-liquid carb HC diet. I blogged on this in a series: Where do Triglycerides Come From? Part I , Part II , Part III. The major contributor to increased VLDL rates was reduced clearance and not increased production by the liver.
What else raises triglycerides? Well ... fructose and alcohol. What do these have in common? Both require "real time" metabolism and reduce LCFA oxidation. MCT's are also metabolized by the liver. There is every reason to believe that this too will take metabolic preference over LCFA oxidation and result in the very same perturbation of the VLDL metabolism seen for the others. Keeping in mind that CO is only 55% MCT's the LCT's that are ingested with them may circulate for quite a bit.
Humans are not ruminants or hind-gut fermenters. To the best of my knowledge our fatty acid synthesis pathways are limited to a few elongations of specific FA's and palmitic/stearic acid synthesis from AcetylCoA. MCT's go right to oxidation.
I'm also not sure if it's ever been studied what percent of MCT's get incorporated into lipoproteins or not. It's my understanding that they are absorbed and transported w/o being incorporated into chylomicrons, go directly to the liver and are metabolized there. So how many chylo remnants and NEFA are MCT's to get repackaged as VLDL? I used to have a wonderful paper on MCT metabolism but I don't recall if it had anything on this. I'll look for it.
Are all elevated triglycerides created equal? I don't think so. On VLC diets, the low trigs may be premature celebration. On a low fat diet they may not be any cause for concern. In the context of the SAD ... they are at very least a concerning biomarker.
My N=1. In Sep 2010, I was at 220lbs (5'11/46yo), started 'paleo'. Got down to 185 and stalled for months. Examined what I thought was paleo, and cleaned it up. Now, I IF from 6pm til 11am, work out around 10am, and don't snack between meals. I'm now down to 172. During that time, I added considerable muscle and my labs are all right in the middle of normal for everything I've been tested for. I went from taking a handful of various pills for neolithic metabolic derangements to no meds. Things that really helped break the stall were cutting out all sugar-alcohol snacks, eating a bigger lunch than dinner, and not counting macronutrients. I think when I was counting, it made me want to add food I didn't necessarily want or need, but it was all about the percentages.
Travis - Regarding your comment here, I find this blurb on page 2 of particular interest:
After absorption, medium-chain fatty acids exit the enterocyte via the portal circulation and are transported to the liver. Medium-chain fatty acids are essentially oxidized to acetyl-CoA within the hepatic mitochondria (Foufelle et al. 1992). The acetyl-CoA generated may not be completely converted into CO2 and ketone bodies, but a portion of it may serve as substrate for fatty acid synthesis (Geelen 1994). To process the extra acetyl-CoA, the consumption of medium-chain fatty acids could be associated with elevated postprandial activities of acetyl-CoA carboxylase and diacylglycerol acyltransferase which in turn would explain the earlier observed (Van Lith et al. 1990) rise in plasma triacylglycerol.
It seems that the increased oxidation of MCTs to acetyl-CoA could cause a marked increase in triglycerides.
2 things come to mind:
How come my trigs were 85 after 2 months of coconut oil consumption back in Oct 2010?
How come so many other Paleos can eat gobs of CO and maintain superstar trig levels?
Am I the only Paleo that was experimenting with a high fat, moderate starchy carb diet that included coconut oil AND weight lifting 5x per week?