In "The Fat of the Land", Stefansson makes a couple of interesting points which have been tracking for some time.

He makes the following points:
1. Fresh raw to medium rare meat cures and prevents scurvy
2. Meat cooked to shreds does not
3. Salted meat does not

Unfortunately as an early 20th century anthropologist, he offers virtually no biochemical explanation for these phenomena.

He suspected that fresh meat must contain AA, but I've never seen any data that indicates that meat has anything other than small amounts of AA. Although AA is heat sensitive, I don't know how to fares during salt curing, anyone know?

Meat does contain hydroxylysine and hydoxyproline which are precursors to collagen and fibrin, but I've not been able to find good data on exactly how much HL/HP is in various types of meat. I also cannot find data about whether HL/HP survives the stomach and makes it into the blood. Nor can I find data about the effect of salt curing on HL/HP. Any one seen any data about these two points?

The other problem of course is that while meat may prevent acute scurvy, there is no data to answer the question of whether it would prevent chronic scurvy like atherosclerosis. I suspect that a meat-based diet, as practiced by ancient primitives, probably lead to excellent overall health and longevity.

Do you know where I can find data on AA levels in meat?
I find lots of data that indicate there is little to no AA in raw meat. I can find a handful of studies that show there are small amounts of AA in meat.

Can you explain how salt curing destroys AA or blocks it's assimilation?

aariel,

There may also be a difference between vegetarian non-organic fed beef, grass fed beef, and normal supermarket non-organic beef. Then what about various other meats, as poultry, fish, or even other red meats like Ostrich?

Link works fine--thanks.

In primitive, hunting based cultures, the majority of calories will come from fat. Then organ meats and finally muscle meat. While they eat muscle meat, yhey often discarded it or fed it to their dogs. They eat animals very differently than we do. I don't recall seeing AA in animal fat. Organs are not eaten universally. For example, Caribou don't have a gall bladder so bile is stored in the liver. This makes the liver taste bitter so it is only eaten under duress. The table shows minor amounts of AA in small glands that may or may not have even been eaten and even if they were the amount is minimal. There is no way that you can get anything like 3-9g per day eating any part of an animal, or plants for that matter.

I don't question AA efficacy, what I question is if it is the only substance that can perform the many important functions of AA, like building collagen. Since we've had this genetic defect for so long we've surely developed many physiological and behavioral ways to compensate. L-DHA recycling and atherogenisis being two, and an animal based diet that provides ample hydroxylated lysine likely being another.

Back in the day, salted meat would not be heated, especially if it's not smoked (think Prosciutto).

I'm wondering if perhaps it has something to do with the salt itself, but with drying and subsequent oxidizing of AA. Although it appears that L-DHA recycling may render this whole theory moot. Although I don't know enough about the chemistry. Perhaps AA oxidizes into something that we can't recycle in salted/dried meat.

When AA oxidizes, does is always form L-DHA? or does it produce many products that vary based on what oxidized it?

So it looks like L-DHA is one product of oxidation among many.
I wonder if they've looked at other oxidation products to see if they can be recycled as well?

Clearly recycling has limitations otherwise scurvy wouldn't be a problem.