Vitamin E for Circulation

Vitamin E may help improve or maintain healthy circulation by affecting cholesterol and blood clotting activity in your blood vessels. Vitamin E also has antioxidant properties that may inhibit the onset of atherosclerosis, a condition that occurs when your arteries harden and circulation diminishes. Sufficient vitamin E intake might also prevent or delay coronary heart disease. The Office of Dietary Supplements recommends that adults get 15 mg. of vitamin E per day.

ICAM1

Vitamin E inhibits the activity of protein kinase C, an enzyme that controls functions of other proteins. PKC is required for producing intracellular cell adhesion molecule-1. A March 1999 "Molecular Pharmacology" study led by Arshad Rahman, of the University of Illinois, treated human pulmonary artery cells with a PKC inhibitor. The treatment prevented ICAM-1 transcription, which the processes of copying genetic information to produce new molecules. Vitamin E promotes circulation, because preventing ICAM-1 transcription limits the adhesiveness of the interior wall of your blood vessels. For example, LFA-1 is a molecule that becomes active when it binds with ICAM-1, and active LFA-1 clogs blood vessels by causing an instantaneous aggregation of circulating cells.

VCAM1

Vitamin E promotes circulation by reducing the activity of vascular cell adhesion molecule-1, a protein that regulates the adhesion of other molecules to the interior surface of your blood vessels. A May 2001 "Journal of Clinical Investigation" study led by Myron Cybulsky, of the Toronto General Research Institute, drastically reduced the activity of VCAM-1 proteins and VCAM-1 transcription in genetically altered mice. The mice were put on a cholesterol rich diet for eight weeks. Atherosclerotic lesions, plaques that clog arteries, reduced by 40 percent in the genetically altered mice. The researchers concluded that VCAM-1 plays a significant role in early stages of atherosclerosis, because the plaque reduction was pronounced in areas affected at the onset of atherosclerosis.

CPLA2

Vitamin E promotes the activity of cytosolic phospholipase A2, an enzyme that releases stored fatty acids including arachidonic acid. Arachidonic acid is converted to prostaglandin endoperoxide, which is then converted into prostacyclin by prostacyclin synthase enzymes. Vitamin E can improve circulation, because increasing prostacyclin suppresses the aggregation of platelets that accumulate in blood vessels and clot your blood. Prostacyclin also helps prevent cholesterol build up inside blood vessels, and helps break down blood clots in atherosclerotic patients.

COX1

Vitamin E supports cyclooxygenase-1 activity. COX-1 is an enzyme that is responsible for the formation molecules that regulate biological activity. An October 2008 "FASEB Journal" study led by Chiara Bolego, of the University of Milan, treated human umbilical vein cells with inhibitors that selectively targeted COX-1 and COX-2 enzymes. Both treatments reduced prostacyclin production that is normally induced by interleukin-1, a protein that regulates inflammatory responses. However, only COX-1 inhibition decreased prostacyclin production in the presence of two fatty acids, arachidonic acid and 12-hydroperoxy-eicosatetraenoic acid. The researchers concluded that COX-1 plays a critical role in prostacyclin production. Vitamin E might improve circulation by promoting prostacyclin production, which markedly improves in the presence of COX-1.