maybe more help re: fluoride detox?

from above link:

"Added supplemental choline and food consumed with drinking
water may help bind up the negative effects of fluoride salts and prevent this from happening."

info on choline. BTW, I see fatty liver mentioned in this link. That's something we've never seen on CZ, huh?

http://lpi.oregonstate.edu/infocenter/othernuts/choline/


Choline

Although choline is not by strict definition a vitamin, it is an essential nutrient. Despite the fact that humans can synthesize it in small amounts, choline must be consumed in the diet to maintain health (1). The majority of the body's choline is found in specialized fat molecules known as phospholipids, the most common of which is called phosphatidylcholine or lecithin (2).

Function

Choline and compounds derived from choline (i.e., metabolites) serve a number of vital biological functions (2-4).

Structural integrity of cell membranes

Choline is used in the synthesis of the phospholipids, phosphatidylcholine and sphingomyelin, which are structural components of all human cell membranes.

Cell signaling

The choline-containing phospholipids, phosphatidylcholine and sphingomyelin, are precursors for the intracellular messenger molecules, diacylglycerol and ceramide. Two other choline metabolites, platelet activating factor (PAF) and sphingophosphorylcholine, are also known to be cell-signaling molecules.

Nerve impulse transmission

Choline is a precursor for acetylcholine, an important neurotransmitter involved in muscle control, memory, and many other functions.

Lipid (fat) transport and metabolism

Fat and cholesterol consumed in the diet are transported to the liver by lipoproteins called chylomicrons. In the liver, fat and cholesterol are packaged into lipoproteins called very low density lipoproteins (VLDL) for transport through the blood to tissues that require them. Phosphatidylcholine is a required component of VLDL particles. Without adequate phosphatidylcholine, fat and cholesterol accumulate in the liver (see Deficiency).

Major source of methyl groups

Choline may be oxidized in the body to form a metabolite called betaine. Betaine is a source of methyl (CH3) groups required for methylation reactions. Methyl groups from betaine may be used to convert homocysteine to methionine. Elevated levels of homocysteine in the blood have been associated with increased risk of cardiovascular diseases (5).

Deficiency

Symptoms

Men and women fed intravenously (IV) with solutions that contained adequate methionine and folate but lacked choline have developed a condition called "fatty liver" and signs of liver damage that resolved when choline was provided (3). Choline is required to form the phosphatidylcholine portion of very low density lipoprotein (VLDL) particles. VLDL particles transport fat from the liver to the tissues (see Function). When the supply of choline is inadequate, VLDL particles cannot be synthesized and fat accumulates in the liver, ultimately resulting in liver damage. Because low density lipoprotein (LDL) particles are formed from VLDL particles, choline-deficient individuals also have reduced blood levels of LDL cholesterol (6). Healthy male volunteers with adequate folate and vitamin B12 nutrition developed elevated blood levels of a liver enzyme called alanine aminotransferase (ALT) when fed a choline-deficient diet. Elevated ALT activity is a sign of liver damage. More recently, a study in 57 adults who were fed choline-deficient diets under controlled conditions found that 77% of men, 80% of postmenopausal women, and 44% of premenopausal women developed fatty liver, liver damage, and/or muscle damage (7). These signs of organ dysfunction resolved when choline was replaced in the diet. Premenopausal women may be relatively resistant to choline deficiency, because estrogen induces endogenous synthesis of choline via the phosphatidylethanolamine N-methyltransferase (PEMT) enzyme (8). Further, recent studies have identified a small number of very common genetic polymorphisms that predict the risk for developing symptoms or organ dysfunction when deprived of dietary choline (9, 10). In choline deficiency, liver damage appears to be the result of increased liver cell death becuase cell culture studies have shown liver cells initiate programmed cell death (apoptosis) when deprived of choline (3). A recent study in 51 men and women reported that a choline-deficient diet induced DNA damage and apoptosis in peripheral lymphocytes (11).

Nutrient interactions

The human requirement for choline is affected by its relationships with other methyl group donors such as folate and S-adenosyl methionine (SAM). See diagram. The methyl group donor (SAM) is synthesized from the amino acid, methionine. Three molecules of SAM are required for the three methylations of phosphatidylethanolamine needed to synthesize phosphatidylcholine. Once SAM donates a methyl group it becomes S-adenosyl homocysteine, which is metabolized to homocysteine. Homocysteine can be converted to methionine in a reaction that requires methyl tetrahydrofolate (THF) and a vitamin B12-dependent enzyme. Alternately, betaine (a metabolite of choline) may be used as the methyl donor for the conversion of homocysteine to methionine (2). For a more thorough discussion of the relationships between homocysteine levels and nutrient intake see the Linus Pauling Institute Newsletter article: The Vascular Toxicity of Homocysteine and How to Control It.

A study of 21 men and women fed diets with varied folate and choline content indicated that choline is used as a methyl group donor when folate intake is low, and that the de novo synthesis of phosphatidylcholine is not sufficient to maintain adequate choline nutritional status when dietary folate and choline intakes are low (12).

why doesnt this work on MY kids! lol