Tuesday, 10 June 2014

Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

The good:

Here's a plot of mean (±SEM) plasma glucose concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal.
From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

An OGTT (100g of glucose dissolved in water) causes a large disturbance in blood glucose level for up to 2 hours. Ditto for insulin (see Fig. 2).

An OFTT (40g of fat as cream) doesn't cause a significant disturbance in blood glucose level. Ditto for blood insulin (see Fig. 2).

The bad:

Here's a plot of mean (±SEM) plasma triacylglycerol concentrations during an oral-fat-tolerance test (OFTT) when preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal.
From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

An OFTT (40g of fat as cream) causes a significant rise in blood triacylglycerol (a.k.a. TAG a.k.a. triglycerides a.k.a. TG's) level for up to 4 hours. Note that the effect of a preceding high-carbohydrate meal on fasting TG's is only +0.1mmol/L. Is high postprandial TG's a problem? Definitely, maybe. From Cholesterol And Coronary Heart Disease , "Cholesterol-depleted particles oxidise faster than large, cholesterol-rich ones." Chylomicrons, chylomicron remnants & VLDL-C are triglyceride-rich, cholesterol-poor, as that's the composition of the fat in the diet.

The ugly:

Here's evidence that excessive postprandial TG's significantly raise the relative risk (RR) for CHD:- See Fig. 1 in Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women.

Here's more evidence that postprandial saturated fatty TG's raise the RR for CHD:- See Postprandial triglyceride-rich lipoproteins promote invasion of human coronary artery smooth muscle cells in a fatty-acid manner through PI3k-Rac1-JNK signaling.

See also Postprandial triglyceride-rich lipoprotein changes in elderly and young subjects.,
Effect of a single high-fat meal on endothelial function in healthy subjects.,
Postprandial lipemia: emerging evidence for atherogenicity of remnant lipoproteins.,
Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men.,
Evidence for a cholesteryl ester donor activity of LDL particles during alimentary lipemia in normolipidemic subjects.,
Association of postprandial hypertriglyceridemia and carotid intima-media thickness in patients with type 2 diabetes.,
Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress.,
High-energy diets, fatty acids and endothelial cell function: implications for atherosclerosis.,
Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates.,
[Influence of postprandial hypertriglyceridemia on the endothelial function in elderly patients with coronary heart disease].,
Impact of postprandial variation in triglyceridemia on low-density lipoprotein particle size.,
Association between fasting and postprandial triglyceride levels and carotid intima-media thickness in type 2 diabetes patients.,
[Correlation of lipemia level after fat loading with manifestation of atherosclerosis in coronary arteries].,
Postprandial hypertriglyceridemia and carotid intima-media thickness in north Indian type 2 diabetic subjects.,
Association between postprandial remnant-like particle triglyceride (RLP-TG) levels and carotid intima-media thickness (IMT) in Japanese patients with type 2 diabetes: assessment by meal tolerance tests (MTT).,
Postprandial lipemia and remnant lipoproteins.
Elevated levels of platelet microparticles in carotid atherosclerosis and during the postprandial state.,
Postprandial metabolic and hormonal responses of obese dyslipidemic subjects with metabolic syndrome to test meals, rich in carbohydrate, fat or protein.,
Atherosclerosis, diabetes and lipoproteins.
Clinical relevance of non-fasting and postprandial hypertriglyceridemia and remnant cholesterol.,
Post-prandial hypertriglyceridemia in patients with type 2 diabetes mellitus with and without macrovascular disease.,
A hypertriglyceridemic state increases high sensitivity C-reactive protein of Japanese men with normal glucose tolerance.,
CD36 inhibitors reduce postprandial hypertriglyceridemia and protect against diabetic dyslipidemia and atherosclerosis.
[Trends of evaluation of hypertriglyceridemia -from fasting to postprandial hypertriglyceridemia-].,
The effects of dietary fatty acids on the postprandial triglyceride-rich lipoprotein/apoB48 receptor axis in human monocyte/macrophage cells.

See also What Is the Significance of Postprandial Triglycerides Compared With Fasting Triglycerides? and Uncovering a Hidden Source of Cardiovascular Disease Risk.

A counter-argument is that the subjects in the above studies were eating carbohydrate, and that postprandial TG's aren't atherogenic if you're not eating much carbohydrate. Definitely, maybe. In the absence of carbohydrate, there is still glucose in the blood, thanks to the liver. Also, some carbohydrates don't spike blood glucose (or fructose) level. It's pure speculation that the subjects in the above studies had high blood glucose at the same time as high postprandial TG's. As Insulin Resistance/Metabolic Syndrome and/or a high-sugar diet raise fasting TG's, and there was no significant association between fasting TG's and the risk factor for CHD, this suggests that the subjects had no significant metabolic derangement and were not eating excessive amounts of sugar.

According to Very Low-Carbohydrate and Low-Fat Diets Affect Fasting Lipids and Postprandial Lipemia Differently in Overweight Men, there's a ~50% reduction in postprandial TG's after adaptation to a very-low-carb, very-high-fat diet. However, mean energy intake was only 1,850kcals/day. The subjects were in a 500kcal/day energy deficit and the %E from fat was only 60%.

Also, some people's LDL levels go extremely high on a very-low-carb, very-high-fat diet. See Lipidaholics Anonymous Case 291 Can losing weight worsen lipids? A very high LDL level results in a high LDL particle count, even if the particles are large (Type A). A high LDL particle count is a strong risk factor for CHD. See also Fig. 1 in Some Metabolic Changes Induced by Low Carbohydrate Diets.

It's possible to get Coronary Artery Calcium (CAC) scans, to measure the amount of calcified plaque in coronary arteries. While a high CAC value means lots of plaque, a zero CAC value doesn't necessarily mean zero plaque, as young people and people with a high Vitamin K2 intake don't have significant calcification. See Stenosis Can Still Exist in Absence of Coronary Calcium.

Update 26th July 2014: See Page 10 of  HIGH CARBOHYDRATE DIETS: MALIGNED AND MISUNDERSTOOD - Nathan Pritikin. Read the text, starting with:-
"Could such a cream meal precipitate an angina attack because the oxygen-carrying capacity of the blood is lowered?"
The answer appears to be "Yes."

12 comments:

Galina L. said...

I always though we all will be better off without evening meals. Most of the time my family has a salad for our dinner.
Nigel, I think that frequency of eating also plays a role, and many LCarbers skip meals and don't snack.

Nigel Kinbrum said...

Hi Galina,
You're not an ~80% fat diet as far as I know, so you should be O.K.

aicha said...

text with the curve you try to clarify something

fredhahn said...

Galina - Nigel's hypothesis has as many holes as swiss cheese. Don't worry about high fat, low carb meals - in my opinion the science does not support Nigel's poorly formulated opinion.

Nigel Kinbrum said...

Fredrick Hahn,

You don't get to slag me off on my own blog. Welcome to my Black-list!

Cheers, Nige

CynicalEng said...

So the fasting TAG levels were higher when preceded by a high carb evening meal, P < 0.001, and were also higher after the OGTT and OFTT where the preceding evening meal was high carb http://ajcn.nutrition.org/content/75/3/505/F3.expansion.html - all of which points to the evening meal being high fat producing many hours of lower TGs overnight and through the tests.

This seems more relevant in the real world than the PP TGs of an OFTT ?

CynicalEng said...

It was 0.2 or 20% more TAG at fasting, really need the AUC data which they didn't provide. The post prandial TAGs from the evening meal looks more interesting than an artificial OFTT although even that was worse when preceded by the high carb meal. If "triglyceride levels measured 2 to 4 hours postprandially had the strongest association with cardiovascular events" then a cup of cream doesn't look good compared to a cup of glucose syrup on a regular basis.

Nigel Kinbrum said...

"If "triglyceride levels measured 2 to 4 hours postprandially had the
strongest association with cardiovascular events" then a cup of cream
doesn't look good compared to a cup of glucose syrup on a regular basis."
Exactly. Not that I would advise anybody to regularly drink cups of glucose syrup. If 40g of fat raises PP TAGs by 0.6mmol/L, what will 100g fat do? Higher, or the same level but for longer? Either way, mean plasma TAGs are elevated more by 100g of fat than 40g. If somebody eats only 2 meals a day on a 80%E fat diet, each meal could easily contain 100g of fat.



Have you read the studies at the end? There are mechanistic explanations as to why PP TAGs are bad for arteries.

CynicalEng said...

Cream is fat largely without protein so an assessment of an 80%E diet should probably use an 80% test meal where the protein response to the insulin will perhaps change the picture.

http://jn.nutrition.org/content/134/4/880/F1.expansion.html shows how after 6 weeks on a hypocaloric diet the PP TAG response to an 86% fat meal is muted compared to baseline and different depending on diet composition.

Nigel Kinbrum said...

Good find! From http://jn.nutrition.org/content/134/4/880.full
"Postprandial lipemia (total AUC) was significantly reduced by both diets
compared with baseline (22.1 ± 5.4 mmol/L × 8
h), but the reduction was significantly greater
after the very low-carbohydrate diet period (13.8 ± 3.6 mmol/L × 8 h)
compared
with the low-fat diet period (17.8 ± 6.0 mmol/L × 8
h). Compared with baseline, peak TAG responses were also significantly
reduced after the very low-carbohydrate (−34%) and
low-fat (−23%) diet periods."
The OFTT AUC for very low-carbohydrate was 32.5% lower than the OFTT AUC for low-fat, and the peak TAG was reduced from 2.45mmol/L to 2.05mmol/L, a reduction of 16.7%.
That's not exactly what I'd call "muted", but it's significantly lower.

My point is, if doubling the amount of fat in a meal results in a 100% increase in the PP TAG AUC, a 16.7% reduction due to fat adaptation isn't going to help much.

CynicalEng said...

A more representative mixed meal scenario at http://www.lipidworld.com/content/10/1/106/figure/F1 shows a broadly similar TAG rise, to answer my own query about mixed meal effect.

Nigel Kinbrum said...

Test meal composition, from Table 3:-
"47g fat, 23g protein, 69g carbohydrate."
That's 54.7% fat, 11.9% protein, 33.4% carbohydrate. That may explain the slightly smaller PP TAG rise.



~80%E from fat meals would be ~20%E from protein i.e. similar to but higher protein than an OFTT. The extra protein will reduce PP TAG a bit relative to an OFTT.