Folic Acid (B9) 5mg/mL
Folic acid is a water-soluble, B-complex. This vitamin is found in a variety of foods including liver, kidneys, yeast, and leafy, green vegetables. A deficiency in folic acid can cause a variety of hematologic complications including megaloblastic and macrocytic anemias.
In recent years, it has been discovered that adequate folic acid intake can substantially decrease the risk of congenital neural tube defects.
An important role of folic acid is the formation of methionine from homocysteine using vitamin B12 as a cofactor.
Adequate folic acid intakes can normalize high homocysteine levels via increased trimethylation of homocysteine to methionine via 5-methyltetrahydrofolate-homocysteine methyltransferase (a.k.a.; methionine synthetase).
Reduced folic acid intake is associated with hyperhomocysteinemia. Hyperhomocysteinemia is recognized as an independent risk factor for atherosclerosis of the coronary, cerebral, and peripheral vasculature.
There is mounting evidence that elevated plasma homocysteine (and therefore decreased serum methionine) contributes to congenital neural tube defects.
High serum homocysteine levels may also be important in the pathogenesis of colon cancer, diabetic retinopathy, and other diseases.
Folic acid is a water-soluble, B-complex. This vitamin is found in a variety of foods including liver, kidneys, yeast, and leafy, green vegetables. A deficiency in folic acid can cause a variety of hematologic complications including megaloblastic and macrocytic anemias.
In recent years, it has been discovered that adequate folic acid intake can substantially decrease the risk of congenital neural tube defects.
An important role of folic acid is the formation of methionine from homocysteine using vitamin B12 as a cofactor.
Adequate folic acid intakes can normalize high homocysteine levels via increased trimethylation of homocysteine to methionine via 5-methyltetrahydrofolate-homocysteine methyltransferase (a.k.a.; methionine synthetase).
Reduced folic acid intake is associated with hyperhomocysteinemia. Hyperhomocysteinemia is recognized as an independent risk factor for atherosclerosis of the coronary, cerebral, and peripheral vasculature.
There is mounting evidence that elevated plasma homocysteine (and therefore decreased serum methionine) contributes to congenital neural tube defects.
High serum homocysteine levels may also be important in the pathogenesis of colon cancer, diabetic retinopathy, and other diseases.
Folic acid is a water-soluble, B-complex. This vitamin is found in a variety of foods including liver, kidneys, yeast, and leafy, green vegetables. A deficiency in folic acid can cause a variety of hematologic complications including megaloblastic and macrocytic anemias.
In recent years, it has been discovered that adequate folic acid intake can substantially decrease the risk of congenital neural tube defects.
An important role of folic acid is the formation of methionine from homocysteine using vitamin B12 as a cofactor.
Adequate folic acid intakes can normalize high homocysteine levels via increased trimethylation of homocysteine to methionine via 5-methyltetrahydrofolate-homocysteine methyltransferase (a.k.a.; methionine synthetase).
Reduced folic acid intake is associated with hyperhomocysteinemia. Hyperhomocysteinemia is recognized as an independent risk factor for atherosclerosis of the coronary, cerebral, and peripheral vasculature.
There is mounting evidence that elevated plasma homocysteine (and therefore decreased serum methionine) contributes to congenital neural tube defects.
High serum homocysteine levels may also be important in the pathogenesis of colon cancer, diabetic retinopathy, and other diseases.