Choline affects heart health through a variety of mechanisms.
First, it lowers homocysteine levels which cause oxidative stress and damage to LDL cholesterol, leading to plaque formation. Choline also works to support a strong heart muscle with regular contractions, leading to a controlled and lower heart rate with less stress to the heart over time.
Homocysteine is a metabolically-generated amino acid which is directly and inversely associated with choline intake (Cho et al, 2006; McCully, 1998; Olthof et al, 2005; Verhoef, 2005). High circulating levels of homocysteine are associated with oxidative events, such as an increase in reactive oxygen species, spurring the oxidation of low density lipoproteins, DNA damage, the rampant growth of smooth muscle cells, and aggregation of platelets that result in occlusive damage to tissues and organs (Ulrey et al, 2005; Garcia and Zanibbi, 2004; Kang, 1996). Higher levels of choline intake lower homocysteine levels through a two-step oxidation process, subsequently methylating homocysteine to S-adenosylmethionine. S-adenosylmethionine acts as a methyl donor necessary for the synthesis of DNA and RNA, the myelin insulation for neurons and other materials. (Lokk, 2003; Ulrey et al, 2005).
The heart is a strong muscle, a little bigger than a fist. The American Heart Association states that, during the day, the average heart beats 100,000 times and pumps about 2,000 gallons of blood. The heart has four chambers -- two atriums and two ventricles -- that open and close in a specific rhythm, which is controlled by electrical impulses. According to the American Heart Association, heart chambers contract when an electrical impulse moves across them. This movement triggers the sinoatrial node, or the "pacemaker," to send out impulses, which in turn cause the heart to beat. The built-in pacemaker generates impulses at a steady rate; however, emotions, actions, and hormonal factors can cause the heart rate to vary.
Acetylcholine is a neurotransmitter used by nerve cells that control the heart, muscles, and lungs. Acetylcholine supports communication between nerves and the heart muscle. Acetylcholine is released at the junction between nerve and muscle cells, called the motor end-plate. This release signals calcium ions to begin muscle contraction.
The heart receives its electrical impulses via the vagus nerve and sympathetic nervous system fibers. The right vagal nerve primarily innervates the sinoatrial node, which is under parasympathetic nervous system control. The parasympathetic nervous system governs "at rest" behavior, like digestion, whereas the sympathetic nervous system is your body's stress response. In other words, the sympathetic response leads to a racing heart, while the parasympathetic maintains your body at rest.
It is parasympathetic and vagus nerve activation that releases acetylcholine into the sinoatrial node. This action decreases the pacemaker rate by increasing potassium and decreasing calcium and sodium movement. As the pacemaker slows, so does heart rate. At rest, the acetylcholine released by the vagus nerve reduces the heart rate.
Cho E, Zeisel SH, Jacques PF, Selhub, J, Dougherty L, Colditz, GA (2006) Dietary choline and betaine assessed by food frequency questionnaire in relation to plasma total homocysteine concentration in the Framingham Offspring Study. Am J Clin Nutr 83:905-11.
Garcia A and Zanibbi K (2004) Homocysteine and cognitive function in elderly people. Can Med Assoc J 171(8):897-904.
Kang SS. (1996) Treatment of hyperhomocyst(e)inemia: physiological basis. J Nutr 26(4 Supple):1273S-5S.
Lokk J (2003) Association of vitamin B12, folate, homocysteine, and cognition in the elderly. Scand J Nutr 47(3):132-8.
McCully KS (1998) Homocysteine and vascular disease: the role of folate, choline, and lipoproteins in homocysteine metabolism. In: Zeisel SH, Szuhaj BF editors. Choline, Phospholipids, Health and Disease. Champaign, IL: AOCS Press, pp. 117-30.
Olthof MR, Brink EJ, Katan MB, Verhoef P (2005) Choline supplemented as phosphotidylcholine decreases fasting and postmethionine-loading plasma homocysteine concentrations in healthy men. Am J Clin Nutr 82:111-7.
Ulrey CL, Liu L, Andrews LG, Tollefsbol TO (2005) The impact of metabolism on DNA methylation. Hum Molec Genetics 14(Review Issue 1):R139-R147.
Verhoef, P deGroot LCPGM (2005) Dietary determinants of plasma homocysteine concentrations. Seminars in Vascular Medicine 5(2):110-23.