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What is Homocysteine & How Is It Related to Cardiovascular Disease


What is Homocysteine & How Is It Related to Cardiovascular Disease

Cardiovascular conditions affect one third of the population worldwide and  have remained among top concerns in the medical society. Alongside of medical advancements, surgical techniques and drugs, safe and effective preventive methods provide the most suitable way for the reduction in Cardiovascular Disease (CVD). A healthy lifestyle including physical activity and stress management, nutrition, and the elimination of the risks of atherosclerosis (smoking, diabetes, hypertension, obesity, elevation of plasma cholesterol, and homocysteine) all contribute to the primary prevention of CVD. As an example, elevated Homocysteine is considered as a risk factors to Cardiovascular Disease while it can be lowered and kept at the safe levels to prevent the arterial damage and its unwanted adverse effects.

What Is Homcysteine?

Homocysteine is a sulfur (sufhydryl) containing amino acid which is naturally produced as a result of our body using dietary amino acid Methionine to produce amino acid Cysteine. Methionine is an essential amino acid for human and found in high amount in animal proteins including meat, egg, and dairy products.  In the event of Methionine deficiency, Homocysteine can be recycled to make more Methionine, while in the presence of enough Methinine, it will be turned into Cysteine.

High blood level of Homocysteine (hyperhomocysteinemia) may arise from genetic defects of enzymes involved in homocysteine metabolism and/or from nutritional deficiencies of folate, vitamin B6, and vitamin B12. In addition; several diseases such as kidney and thyroid disorders, cancer, psoriasis, and diabetes as well as some types of drugs, alcohol, tobacco, coffee, older age and menopause, are found to be associated with moderately high homocysteine level. High serum creatinine is an indicative of kidney disease which is also leads to elevated fasting total homocysteine.

Plasma homocysteine is mainly cleared via kidneys, therefore any kidney disorder may impact the homocysteine blood concentrations. Total homocysteine levels are found to be considerably higher in patients with chronic renal disease. Plasma homocysteine can be increased by drugs and diseases that interfere with metabolism and or absorption of B vitamins especially folate, vitamin B6, and B12.

Correlation Between High Blood Homocysteine Level & Cardiovascular Disease

Homocysteine is known as an independent risk factor for Atherosclerosis (hardening of the arteries). Also; higher blood homocysteine level enhances the adverse effects of cardiovascular disease risk factors such as high blood pressure, high blood lipids, smoking, as swell as promoting progress of inflammation.

Cardiovascular disease includes the health conditions related to the heart and blood vessels, and it is cause of one third of deaths globally. Atherosclerosis is a continuous inflammation of the inner arterial walls with an increase in their permeability causing deposition of plasma lipids and calcium which eventually forms plaques. Atherosclerosis is the most common path to Cardiovascular Disease.

In several studies blood homocysteine level of patients with coronary artery disease was significantly higher than patients without coronary artery disease; in addition, findings show higher homocysteine levels are significantly related with severity of coronary artery disease, arterial stiffness, and high blood pressure.

How Does Homocysteine Cause Cardiovascular Disease?

Homocystein impacts vascular endothelium and their smooth muscle cells altering arterial structure and function. It increases cellular division of vascular smooth muscles, causes endothelial dysfunction, increases oxidative damage, alters collagen synthesis and deteriorates arterial wall elasticity.

Studies demonstrated that homocysteine is able to initiate an inflammatory response in vascular smooth muscle cells by stimulating CRP (an inflammatory marker) production.

High homocysteine level contributes to lower endothelial production and bioavailability of nitric oxide which is a strong relaxing factor for vessels. There is also a strong evidence that increased homocysteine level promotes oxidation. Other studies found that Homocysteine promotes coagulation process.

Another common cause of the cardiovascular diseases is high blood pressure or hypertension. While multiple factors may contribute to the development of hypertension, the association of homocysteine with blood pressure deserves to be noted.

Experimental and animal studies show that the high blood pressure could result from high blood homocysteine. Homocysteine may elevate blood pressure through different ways such as its adverse effect on the integrity of vascular endothelium, oxidative stress, and reduced available nitric oxide (vasodilator). Observational human studies found vasodilation impairment in both temporary and chronic cases of hyperhomocysteinemia (High blood Homocysteine level). Homocysteine has been positively linked to both high diastolic and systolic blood pressure.

Homocysteine Levels & Its Impact On The Brain & Nervous System

In the recent years, epidemiological studies have found an association between homocysteine level and neurodegenerative disorders. These studies suggest that homocysteine can initiate nerve damage though oxidative process, DNA Damage, and promoting self death in neurons cells. Also an increase in the amount of Homocyteine after head injuries and stroke is related to release of catecholamines. High catecholamine levels in blood are associated with stress and depression. Catecholamines are also play an important role in regulating heart rate, blood pressure, and blood glucose.

Brain can only metabolize the Homocysteine by converting it back to Methionine using an enzyme called Methionine synthase. For this Enzyme to work adequate amount of methylcobalamin ( B12 ) and folate is necessary. It should be noted that the level of 5 tetrahydrofolate (5 MTHF- biologically active for of folate) in the cerebrospinal fluid is 3 times that of the plasma level.

In a clinical study patients with major depressive disorder were prescribed 8 weeks of treatment with biologically active form of b vitamins which included 5 MTHF. The Montgomery-Asberg Depression Rating Scale (MADRS) used to evaluate the effect of the treatment. Of the active treatment group 82.4% showed a reduction in homocysteine and demonstrated, on average, a 12-point reduction on the MADRS by week 8, and 42% achieved full remission. These results support the theory of relation between homocysteine levels and depression and the safety and therapeutic benefit of active form of B vitamins, particularly in those cases with deficiencies or a some degree of metabolic and genetic disorders.

Folic Acid, B6, B12 Vitamins, and Arterial Plaque Formation

The process of forming plaques in the inner lining of arteries is referred to as Atherogenesis. Vascular cells, particularly vascular endothelial cells are especially vulnerable to high levels of Homocysteine, because they are not equipped by the diversity of enzymes found in the liver to metabolize or reverse production of the homocysteine in different ways.

The endothelia cells are only rely on the re-methylation pathway of converting homocysteine to methionine. This pathway is Folate and vitamin B12 dependent. Folic acid and vitamins B12 and B6 are important regulators of Homocysteine metabolism. B-vitamins, especially Folate is able to reduce plaque formation by lowering homocysteine level, inhibiting production of superoxide (free radicals), and increasing the half life of Nitric Oxide (main vasodilator).

Maintaining moderate-to-high serum folate levels have been shown to be associated with a great reduction in acute coronary events; and an increased intake of Folate has been associated with a decreased risk of ischemic stroke. A study of 26,556 smoker men between 50 to 69 years of age showed that higher intake of Folate contributed to statistically significant lower risk of stroke.

Several trials and studies support the beneficial effects of B-vitamin supplementation in the prevention of Cardiovascular Disease. A Swedish study found that a daily use of multivitamin supplementation (containing 400 mcg of Folate) reduced risk of MI (Myocardial infarction) in women without the previous history of Cardiovascular Disease. According to the conclusion of the study, multivitamin supplementation may help in primary prevention of MI.

Meta Data analysis of multiple trials suggests that a number of the trials using B vitamin therapy were effective in reducing the risk of stroke, and long-term vitamin B supplementation may be effective in the primary prevention of Cardiovascular Disease. Primary prevention indicates for those without the previous history of Cardiovascular Disease.

The use of B-vitamins for secondary prevention could be an option to prevent the progress of the disease and when statin therapy caused serious adverse effects and should be omitted. Vitamin B therapy may inhibit the progression of atherogenesis by lowering Homocyteine and by other mechanisms such as through its antioxidant properties.

The evidence from studies published over the last two decades suggests that the B vitamin therapy offers an inexpensive, nontoxic, and easy method of primary Cardiovascular Disease prevention and secondary prevention by limiting the progression of the disease due to risk factors such as Homocysteine.

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