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Nutrition in Stroke Prevention
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Nutrition is far more important than most physicians and patients recognize. Maintaining a healthy weight, reducing dietary cholesterol, avoiding egg yolks, and consuming a Cretan Mediterranean diet substantially reduce the risk for stroke. Besides the very high cholesterol content of egg yolks (more than the recommended daily intake of 200 mg of cholesterol in a single large egg yolk), it is now apparent that phosphatidylcholine (lecithin, 250 mg per egg yolk) is converted by intestinal bacteria to trimethylamine, which in turn is oxidized in the liver to trimethylamine n-oxide (TMAO), which is pro-atherosclerotic in animal models and increases the risk for cardiovascular events in patients at risk for coronary disease. Unrecognized metabolic deficiency of vitamin B12 is very common, and frequently missed, because a normal serum B12 is not a reliable test for adequacy of B12. Besides neuropathy, myelopathy, and dementia, B12 deficiency increases the risk for stroke by raising levels of total homocysteine (tHcy). Despite widespread misunderstanding of the complex issues, it is increasingly clear that B vitamin therapy to reduce homocysteine does reduce the risk for stroke. However adequacy of B12 dosing and renal impairment determine the response to B vitamin therapy: cyanocobalamin is beneficial in patients with normal kidney function, but harmful in those with renal impairment (GFR<50). Methylcobalamin should be used in patients with renal impairment.
Title: Nutrition in Stroke Prevention
Description:
Nutrition is far more important than most physicians and patients recognize.
Maintaining a healthy weight, reducing dietary cholesterol, avoiding egg yolks, and consuming a Cretan Mediterranean diet substantially reduce the risk for stroke.
Besides the very high cholesterol content of egg yolks (more than the recommended daily intake of 200 mg of cholesterol in a single large egg yolk), it is now apparent that phosphatidylcholine (lecithin, 250 mg per egg yolk) is converted by intestinal bacteria to trimethylamine, which in turn is oxidized in the liver to trimethylamine n-oxide (TMAO), which is pro-atherosclerotic in animal models and increases the risk for cardiovascular events in patients at risk for coronary disease.
Unrecognized metabolic deficiency of vitamin B12 is very common, and frequently missed, because a normal serum B12 is not a reliable test for adequacy of B12.
Besides neuropathy, myelopathy, and dementia, B12 deficiency increases the risk for stroke by raising levels of total homocysteine (tHcy).
Despite widespread misunderstanding of the complex issues, it is increasingly clear that B vitamin therapy to reduce homocysteine does reduce the risk for stroke.
However adequacy of B12 dosing and renal impairment determine the response to B vitamin therapy: cyanocobalamin is beneficial in patients with normal kidney function, but harmful in those with renal impairment (GFR<50).
Methylcobalamin should be used in patients with renal impairment.
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