Lead researcher Dr Ira Tabas said that previous research had suggested that this mechanism might be involvedin plaque rupture, but the magnitude of the effect uncovered in the latest study was a surprise.
He said: "The fact that we were able to isolate one gene encoding one protein with such a profound effect on plaque necrosis (death) was a big surprise."
Dr Tabas said the finding raised hopes of new drugs which could act on the key gene, or the associated mechanism, to cut the risk of dangerous plaques.
"Just about everybody in our society has atherosclerosis (thickening of the arteries) by the time we reach 20," he said.
"So the wave of the future in treating atherosclerosis will be in preventing harmless lesions in young people from becoming dangerous ones, or soothing dangerous plaques so they don't rupture as we age."
Never mind what effect such a treatment might have on necessary cell death (e.g. to deal with emerging cancers) in other parts of the body.
Anyway, what does this have to do with diet and the heart? Well, again from the BBC article:
Scientists have identified a genetic mechanism which appears to determine which fatty deposits in the arteries have the potential to kill us. Most of these plaques pose no risk to health, but a minority burst, forming blood clots, which can cause heart attacks or strokes. .....
Fatty deposits begin to form in the arteries of most people in their teens, but the vast majority are harmless.
But, ah you say, just read on ...
The researchers bred mice prone to develop plaques, and fed them a high-fat diet for 10 weeks.
So what was this high-fat diet? It was the TD.88137 Western Diet (Teklad Lab Animal Diets, Harlan Laboratories, Madison, WI) which consists of:
g/kg | |
---|---|
Casein | 195.0 |
DL-Methionine | 3.0 |
Sucrose | 341.46 |
Corn Starch | 150.0 |
Anhydrous Milkfat | 210.0 |
Cholesterol | 1.5 |
Cellulose | 50.0 |
Mineral Mix, AIN-76 (170915) | 35.0 |
Calcium Carbonate | 4.0 |
Vitamin Mix, Teklad (40060) | 10.0 |
Ethoxyquin, antioxidant | 0.04 |
(Data from this pdf.)
How does this compare to a mouse's real diet?
In short, the typical composition of a diet of invertebrates is high in fat and protein e.g. from p.41 in Marsupial nutrition, (Ian D. Hume, Cambridge University Press, 1999) it can range from 20-60% fat and 10-75% protein (by weight of dry matter) for typical things that a mouse might eat (insects and insect larvae). Cereals are typically 68-79% carbohydrate, around 10-15% protein and 2-7% fat, legumes are as much as 25% protein, typically 50-60% carbohydrate and only 1-2% fat whereas nuts (e.g. hazelnut) and oilseeds (e.g. sunflower) are typically about 15-25% protein, 50-60% fat and 15-20% carbohydrate (from various tables in On Food and Cooking, H. McGee, 1st ed. Unwin Hyman, 1984).
From this we can conclude that a typical wild mouse would for part of the year eat a diet that was mainly protein and fat and for another part of the year eat a diet that was high in carbohydrate - at least if it ate cereals, but not so much if it ate other types of seeds - but low in fat. It would not however be eating a lot of sucrose. The carbohydrate in grains and seeds is starch which is a polymer of glucose and does not contain fructose. As further support of this analysis here Peter of Hyperlipid considered data on what wild-type mice eat when given free choice: about 12% protein, 6% carbohydrate and 82% fat (all as proportions of energy).
A final note about the mice. The mice used in the experiment were either apoe or ldlr mice. Apoe mice lack a particular lipoprotein (apolipoprotein E) which is important in both the HDL and vLDL cholesterol transporters, in particular:
ApoE mediates high affinity binding of chylomicrons and vLDL particles to the LDL receptor, allowing for specific uptake of these particles by the liver, preventing the accumulation of cholesterol rich particles in the plasma
.....
Mice develop normally, but exhibit five times normal serum plasma cholesterol and spontaneous atherosclerotic lesions
Does this not indicate that fat is the root cause? Well not necessarily.
So which is more likely to contribute to the problem - the 21.2% of food (by weight) that comes as fat (most of which doesn't go straight to the liver anyway) or the 48.5% of food (by weight) that comes as carbohydrate - three-quarters of which is sucrose and half of that is fructose (i.e. 17% by weight of the total food intake) which goes straight to the liver and comes out as triglycerides.
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