las

Welcome all seeking refuge from low carb dogma!

“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
~ Charles Darwin (it's evolutionary baybeee!)

Saturday, May 21, 2011

Triglycerides: Atherosclerotic or SAD-context Biomarker?

Something that's been on my mind a lot over the past couple of years is the meaning of fasting triglycerides in the context of a low carbohydrate diet.  Many, myself included, tend to look at fasting triglycerides and HDL as more important biomarkers and these two both tend to improve rather greatly on a low carbohydrate diet.  But I've always wondered if the reduced triglycerides of LC really indicate a "reduced risk" compared to the generally higher fasting triglycerides of healthy people eating a higher carbohydrate diet.

I blogged recently about triglycerides increasing on a high carb/low fat diet.  Basically, the elevated VLDL in the high carbers was attributed to reduced clearance and not overproduction in the liver.  So I got to asking if it's the triglycerides themselves that are atherogenic or if they are merely indicative of an underlying pathology.



The fact that carbohydrate-rich diets often increase plasma triglycerides has led some to question the wisdom of such diets. This increase is primarily attributable to a decrease in the efficiency of triglyceride clearance -- whereas the elevation of triglycerides observed in insulin-resistant subjects stems mainly from increased hepatic production of VLDL particles. There is growing reason to suspect that the increased coronary risk associated with elevated triglycerides in Western epidemiology reflects the fact that high triglycerides are a marker for insulin resistance syndrome, rather than any inherent pathogenic role of triglycerides per se. Thus, endothelial dysfunction is seen only in those hypertriglyceridemic subjects who are insulin resistant, and is absent in patients whose markedly elevated triglycerides reflect genetically defective lipoprotein lipase activity. Triglyceride levels are relatively high in certain Third World societies which are virtually immune to coronary disease so long as they persist in their traditional very-low-fat diets; in Ornish's celebrated study, a moderate rise in triglycerides coincided with a marked reduction in coronary events. Although the particle size of both LDL and HDL tends to decrease when triglyceride levels are high, it is questionable whether this effect has a major pathogenic impact.

The author does, to this reader, appear to be biased in favor of low fat diets, and works for a diagnostics company - not sure what that might mean.
The one clear drawback of high-carbohydrate diets is a decrease in HDL particle number, resulting from decreased hepatic production of apoA-I; this effect is seen whether or not triglycerides increase. The very favorable effects of very-low-fat, whole food, quasi-vegan diets on LDL cholesterol, insulin sensitivity, and body weight appear to more than compensate for this decrease in HDL; it is notable that HDL levels tend to be quite low in Third World cultures at minimal risk for coronary disease. On the other hand, this decrease in HDL may be of more significance in the context of omnivore diets only moderately low in fat, as suggested by the fact that diets higher in unsaturated fats emerge as more protective in Western prospective epidemiology. The tendency of high-carbohydrate diets to boost triglycerides can be minimized by exercise training, supplemental fish oil, an emphasis on fiber-rich, low-glycemic-index whole foods, and the "spontaneous" weight loss often seen with ad libitum consumption of such diets -- measures which are highly recommendable whether or not triglycerides are a concern.
I am sharing the full text through Google docs:  HERE

The first reference in that article is, no surprise, Parks & Hellerstein on a similar topic:

Carbohydrate-induced hypertriacylglycerolemia: historical perspective and review of biological mechanisms


Current trends in health promotion emphasize the importance of reducing dietary fat intake. However, as dietary fat is reduced, the dietary carbohydrate content typically rises and the desired reduction in plasma cholesterol concentrations is frequently accompanied by an elevation of plasma triacylglycerol.  We review the phenomenon of carbohydrate-induced hypertriacylglycerolemia, the health effects of which are among the most controversial and important issues in public health nutrition today. We first focus on how seminal observations made in the late 1950s and early 1960s became the basis for subsequent important research questions and areas of scientific study. The second focus of this paper is on the current knowledge of biological mechanisms that contribute to carbohydrate-induced hypertriacylglycerolemia. The clinical rationale behind mechanistic studies is this: if carbohydrate-induced hypertriacylglycerolemia shares a metabolic basis with endogenous hypertriacylglycerolemia (that observed in subjects consuming high-fat diets), then a similar atherogenic risk may be more likely than if the underlying metabolic mechanisms differ. The third focus of the paper is on both the positive metabolic changes that occur when high-carbohydrate diets are consumed and the potentially negative health effects of such diets. The review concludes with a summary of some important research questions that remain to be addressed. These issues include the level of dietary carbohydrate that induces carbohydrate-induced hypertriacylglycerolemia, whether the phenomenon is transient or can be avoided, whether de novo lipogenesis contributes to the phenomenon, and what magnitude of triacylglycerol elevation represents an increase in disease risk.

I encourage my readers to read both of these papers.  I'll be blogging a bit on ... you guessed it ... those pesky NEFA's in all of this sometime soon.  Please do add your thoughts in the comments!!

I am tending to believe that very elevated triglycerides are probably indicative of a problem (like the over 300 crowd), but the normal "risk assessment" marker for triglycerides need to be taken into account in the context of one's diet.  In this retard, hypertriglyceridemia is not necessarily pathologic.  The flip side of this is that the very low triglyceride levels celebrated in the VLC community may not be as indicative of improved health per se.



12 comments:

Harry said...

Sorry, I know I'm horribly infantile, but I was ROTFLMAO when I read this (check the spelling on the third word of the penultimate sentence in your post)...

Cheers
Harry

MM said...

CarbSane,

I think Harry may be referring to this sentence. "In this retard, hypertriglyceridemia..." (Last paragraph)

Charles L. Peden said...

This reminds me of the Kitavans. According to Peter at Hyperlipid, the Kitavans had triglycerides of about 149-263 mg/dL (after conversion). This would seem high if taken out of context. But knowing the dietary environment these numbers are pulled from makes a big difference.

It's kind of like understanding the BMI in context of a person being obese or a bodybuilder even though both measures might be the same.

Helen said...

I've wondered about this. I've had low triglycerides all my life, first on a whole-foods diet (without regard to macronutrient proportions), then on a near-Paleo WAPF-inspired diet (on which I quickly gained 20 lbs, and was diagnosed with borderline diabetes, but still had great triglycerides), then on a low-carb, high-fat diet (on which I slowly lost that 20 pounds).

Now I'm on a low-fat diet relatively high in soluble-fiber-rich carbs. I'm curious to find out if it's affected my triglycerides adversely. (Stephan Guyenet claims this effect is only from refined carbs. If so, I'm safe.)

But I'd also wondered if triglycerides (or even, to some degree, HbA1C - obviously, there is a point at which high average glucose becomes damaging in and of itself) are a marker of some other dysfunction, rather than being themselves harmful.

At my diabetes diagnosis my fasting insulin was not elevated, so I'm not sure I'm particularly insulin resistant, though becoming even slightly overweight did not help my impaired glucose control, whatever its cause.

My current diet has been my best so far for both glucose control and weight loss. I've lost another 10 pounds without trying. I now seem to be plateauing at a BMI of 20, and that's fine.

Mirrorball said...

@Helen Was your near-Paleo WAPF-inspired diet high in fat? How was it different from the low-carb, high-fat diet you went on next?
All I want is to plateau at a BMI of 20.

OnePointFive said...

In my case I think that,insulin, or lack of it and the subsequent ketosis and breakdown of fats has something to do with high trigs. On diagnosis with T1 my trigs were 3,19mmo/l (283mg/dl). Two months later with injected insulin , fairly low fat as I was too scared to do anything but follow instructions and about 180-200g a day of relatively unrefined carbs trigs were at 0.84mmol/l (74mg/dl).

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

Hi Mirrorball,

Yes, it was high in fat. I wasn't counting fat grams, but it was definitely high in naturally occurring fat and added fat. I'd really taken the fat-is-good message to heart. I still don't think saturated fat directly causes heart disease, but if it makes you gain weight and worsens your glucose control, I wonder if it could have an indirect effect. I'm not sure everyone would respond the way I did to either the high-fat or low-fat diet. Many people on these blogs claim they had the opposite experience.

CarbSane said...

Oy! Whatta typo. But it's cute so I'll leave it be :)

Helen this is key IMO: I still don't think saturated fat directly causes heart disease, but if it makes you gain weight and worsens your glucose control, I wonder if it could have an indirect effect.

And it seems that postprandial handling of fats is an issue. Since sat fats are a significant portion of the free fatty acids we release from fat tissue, if we don't adequately trap these dietary fats the body could (not sure on that but could) impact us differently.

CarbSane said...

I recently received this in email:

I wonder if you might be able to answer a triglyceride question:

Is there something in dropping from 130g to 30g carbs per day that might make triglcyerides go up, rather than down?

I've previously had great results in cutting trigs from 520 to 92 in one week by cutting carbs and calories. (It was a bit of an ordeal)

Recently, I went from 130g to around 30g carb per day. Blood sugar dropped dramatically: from 109 to 94/82/88/94 over a four week period.

But triglycerides jumped from 110 to 148/146/181/170 over the same period


I have no idea. Anyone?

Nigel Kinbrum said...

I hypothesise that TG-rich, chol-poor LDL particles oxidise more easily/rapidly than TG-poor, chol-rich ones (as cholesterol is an anti-oxidant). As ox-LDL is atherogenic, high serum TGs is therefore pro-atherogenic.

RE Increasing serum TGs on low carb diet: Has exercise volume decreased due to ordeal? Decreased exercise volume reduces uptake of TGs by muscles as they don't need so much fuel.

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