Vitamin D

Here's a long-promised post about Vitamin D.

On the Marshall Protocol, I will have to avoid all sources of Vitamin D, including D-rich foods and sunlight.  The latter will be a challenge in Southeast Texas, and the former isn't easy thanks to industry-wide fortification of dairy foods.

Vitamin D is one of the most widely misunderstood vitamins out there.  First of all, it's not really a vitamin.  It's called a vitamin because when it was first identified in the 1920s, it was thought to be an essential nutrient. In fact, it is not an essential nutrient because the ingested form is really a precursor—or prohormone—to a hormone that can only be created by the body, not ingested. 

The term "Vitamin D" actually refers to several substances, including the one found in fortified foods (D3), the hormonal precursor, called 25-D, and the hormone, which is called 1,25-dihydroxyvitamin D3, or 1,25-D. The hormone is involved in the immune system, but its exact role there and elsewhere is the subject of much debate. Many long-held beliefs about Vitamin D, such as that a deficiency of it leads to Rickets, have been disproved. (That study, from March 2007, confirmed this 2004 study.) A search on PubMed reveals that there is a lot of current research into Vitamin D's functions. Some of it is contradictory, indicating that it is not well understood yet.

What is certain is this: in healthy people, 1,25-D is synthesized by the skin in the presence of sunlight. Just 10 minutes exposure to indirect sunlight once or twice a week is all that is needed by most people, but more sun exposure doesn't lead to too much 1,25-D in healthy people, because the body creates only as much as it needs. Even this is misunderstood, though: the prevailing theory is that direct contact of UVB is needed on the skin to produce 1,25-D. But this is contradicted by the fact that nocturnal mammals, and even some species of fish that live in caves, produce plenty of 1,25-D. In other words, sunlight exposure is not the only mechanism for the body to produce 1,25-D, and is not absolutely necessary.

edited to add: I left out a step. D3, which is ingested, converts to 25-D in the presence of sunlight and also in the liver. 25-D is then converted to the hormone 1,25-D in the skin and in the kidneys.

And that doesn't even begin to address the issue of how much is necessary for health. What's more, the only function of the precursor Vitamin D (i.e., what is found in foods and supplements) is to enable the body to produce 1,25-D. Since, in healthy people, the body does not produce excess 1,25-D no matter how much D3 is ingested, supplementation is usually both harmless and unnecessary.

The rub, of course, is Vitamin D regulation in sick people, not healthy ones.

There are some studies showing that 1,25-D acts as an immunosuppressant. This is why it can make people with immune-related diseases feel better temporarily: feeling bad is a result of the immune system trying to cope with the disease. Shut that function down, and you don't feel bad anymore. But the disease doesn't go away. It's just like taking steroids.

Dr. Marshall believes that all people with Th1 diseases also have a Vitamin D "disregulation." In these people, the body produces too much 1,25-D. A serum D3 test is therefore not a reliable indicator of 1,25-D levels, but 1,25-D tests are rarely performed because they require specialized handling and are only performed in a few labs (two or three in the U.S.). Another reason they are not performed is that all this 1,25-D research is new and so doctors don't know about it—and if they did know about it, they wouldn't know what to do to treat it.

In any event, Dr. Marshall believes that 1,25-D is what enables the cell-wall-decificent bacteria (which he says causes Th1 diseases) to slip into the white blood cells. So reducing the levels of 1,25-D makes it harder for the CWD bacteria to hide, and enables the immune system to start eliminating them. The only way to reduce the level of 1,25-D is to reduce or eliminate ingestion of D3 and avoid sunlight. In time (many months for some people), this lowers the 1,25-D to a point where it both prevents the CWD bacteria from moving in and out of the phagocytes, but also enables the immune system to recognize the CWD bacteria.