I'd just like to run through the effects of saturated fat vs unsaturated fat on the development of Alzheimers disease in a mouse model genetically engineered to be AD prone. Here is the opening sentence of the paper (thanks to Gary for the pdf):
"In Western Society, diets have gradually changed since World War II, with an increase in total caloric intake, saturated fat, and hydrogenated fat, leading to a decrease in the healthier, unsaturated fats."
This statement is frankly wrong. Good start. BTW There's accurate information on changes in fat intake in the American diet here on Stephan's blog.
Next is the methods. They added 2% by weight of chemical grade cholesterol to the diet of the saturated fat group only, none to the PUFA group. This is called failing to control your variables. If I was scrutineering this paper I would have thrown it out at this point. BTW I roughly translated this amount of cholesterol to mean >50 eggs per day for an adult human, but not as eggs, as chemical grade cholesterol. Anyone fancy trying this?
If you look through the table you will see that just under 24% of the "food" by weight was Alphacel. I think this is cotton wool, near enough.
So the "food" components of the diet are 27% by weight fat, 26% by weight starch and 32% by weight, err, sugar (dextrinised starch=sugar). Yummie. So any mouse eating any food must eat LOTS of sugar.
Why is this a problem if you mix it with saturated fat but not with soya oil? Because saturated fat induces insulin resistance.
Why should this be? Because palmitic acid is the primary NEFA released from human adipose tissue during fasting. Think of palmitic as a signal molecule to tell the muscles that inhibition of glucose uptake is needed and to tell the liver that increased gluconeogenesis is required because there is no food coming in.
Because linoleic acid comprises only a small portion of adipose tissue in humans there is no reason why an increase in this fatty acid should signal the need for physiological insulin resistance. Over an evolutionary time scale elevated linoleic acid levels mean nothing except perhaps you found a few nuts. This is not starvation and insulin resistance doesn't need to happen. Other saturated fats seem to do the same as palmitic, certainly coconut oil, fully hydrogenated, seems to do this in these mice. Lipoprotein lipase certainly spills some of the NEFA it releases from chylomicrons in to the general circulation, especially in muscle beds.
So these poor mice are being made insulin resistant, while being fed sugar. Each mouthful combines saturated fat and sugar. Non stop. Whenever they eat anything. Almost as much sugar as someone on the upper end of the sugar intake in the SAD, but with more fat (27% by weight is 54% of calories). Combining insulin resistance with sugar when you are genetically engineered to get Alzheimers does not embody bad luck. Dementia is guaranteed. For a human sugar junkie there is more genetic chance involved and you might just get lucky enough to have a heart attack sooner rather than dementia later...