West, thanks for the link - I haven't visited T-mag in a while

Interesting article, but I do take issue with a few of the comments (although they don't all bare directly on the issue of ASP).

"Next up: Glucagon. Since glucagon is a regulatory hormone responsible for providing energy to the tissues, it is classified as a catabolic hormone. Essentially, glucagon plays Lex Luther to insulin's Superman. To be more specific, glucagon stimulates the breakdown of stored glycogen into glucose in skeletal muscle and in the liver, stimulates the breakdown of fats into fatty acids in adipose tissue, maintains the liver's output of glucose from amino acid precursors, and leads to the formation of ketone bodies from fatty-acid precursors in the liver; all catabolic events designed at dipping into your energy reserves to provide fuel.

Since a protein-only meal increases the release of glucagon (in order to stimulate the liver to produce glucose to normalize blood sugar) and since fat does nothing to directly mitigate the effects of a protein meal on glucagon release while carbohydrates decrease this response, some have speculated that a protein-only meal or a protein-plus-fat meal is a no-no since the glucagon release may promote the manufacture of glucose from all those ingested amino acids.

While this may be true with a high protein diet that also lacks sufficient dietary carbohydrate I believe that the destruction of amino acids will be minimal if the body has sufficient carbohydrate reserves in the liver."

The author is basing this on someone eating carbs (and says so in the next sentence) "In this case, glucagon will tend to make more of the necessary blood glucose from stored glycogen than from ingested amino acids"

LCers have no stored glycogen in their liver or muscles - that's the first stuff to go when you restrict carbs. Glucagon is the primary / dominant hormone when we eat fat for fuel, because we eat protein as well, and because fat has no metabolic impact on anything - it's neutral. He author has his facts straight but he is basing the outcome on a different situation.

He thing that bothered me the most about the article was the information thrown about with nothing backing it up- and the off handed comment like this: "So where's the scientific data? We don't got none. But the theory makes some sense. <insert hairpullingoutsmilieface>

Now the ASP info is something new - to me, but not to science, as they would have us believe. Again, not much info provided. Here's what I've gathered.

Chylomicrons are not prepackaged fats, they are a lipid-shuttling particle made by the body (in the intestines) to transport fats around to the cells, in particular triglycerides, which are used by the cells as energy. The fat in chylomicrons is normally removed by the tissues and cleared from the blood in 4 to 6 hours. However, when the fat removal mechanisms are impaired, as they are in patients with very high triglycerides, it can take days to clear chylomicrons from the blood. In such an overwhelmed chylomicron removal system, every bit of fat that is eaten in the diet is absorbed into the blood, but has nowhere to go. This causes the triglycerides to increase more and more and of course, that's not good. But does increased serum TG mean increased fat storage?

Where does ASP come into this? It's part of the pathway that clears triglycerides from the body. If you're lacking in it, you don't clear them as quickly, if you've got enough, you clear them from the blood. Interestingly enough, studies on what affects ASP production show that neither glucose nor fatty acid have much of an effect on production. However the introduction of external chylomicrons has a marked increase on ASP production.

What's really interesting about this from a LC stand point is that one of the biggest and first changes to happen to us on a cellular level when we start eating fat as our primary macronutrient: Or triglyceride levels drop drastically - usually to well below the norm.

Obviously there's something going on that has yet to be explained I think part of it has got to have something to do with the source of cholesterol / triglycerdies (dietary over endogenous).

Thanks for the read.

Nat