Homocysteine, an amino acid involved in the methylation cycle, plays a significant role in cardiovascular disease (CVD) and neurological disorders. Elevated homocysteine levels, known as hyperhomocysteinemia, are associated with increased risk of CVD, including atherosclerosis, stroke, and heart attacks. Homocysteine can damage endothelial cells, reduce vascular flexibility, and promote inflammation, contributing to the development of CVD. It also affects the nervous system by acting as a neurotransmitter and causing oxidative stress, DNA damage, and neuronal damage. Homocysteine can trigger the release of excitatory amino acids and catecholamines, which may exacerbate neurological conditions. Hyperhomocysteinemia can result from genetic mutations, nutritional deficiencies in folate, vitamin B6, and B12, or environmental factors. It is linked to various cardiovascular and neurological conditions, including hypertension, stroke, and dementia. The SAM-to-SAH ratio, a key indicator of methylation potential, is reduced in hyperhomocysteinemia, leading to decreased methylation and DNA hypomethylation, which can affect gene expression and contribute to disease progression. Homocysteine also influences vascular stiffness and arterial structure, increasing the risk of atherosclerosis and cardiovascular events. Studies show a correlation between elevated homocysteine levels and increased cardiovascular risk, although the exact mechanisms and the extent of its role as a risk factor remain debated. While some research suggests homocysteine is an independent risk factor for CVD, others indicate that its association may be influenced by other factors such as blood pressure and vascular reactivity. Despite these findings, homocysteine is not yet classified as a standard risk factor for CVD in clinical guidelines. However, its potential as a biomarker for cardiovascular disease risk is being explored. Further research is needed to clarify the role of homocysteine in CVD and to determine its utility in risk prediction and management. Nutritional interventions, such as folate and B vitamin supplementation, may help lower homocysteine levels, but their effectiveness in preventing CVD remains a topic of ongoing investigation.Homocysteine, an amino acid involved in the methylation cycle, plays a significant role in cardiovascular disease (CVD) and neurological disorders. Elevated homocysteine levels, known as hyperhomocysteinemia, are associated with increased risk of CVD, including atherosclerosis, stroke, and heart attacks. Homocysteine can damage endothelial cells, reduce vascular flexibility, and promote inflammation, contributing to the development of CVD. It also affects the nervous system by acting as a neurotransmitter and causing oxidative stress, DNA damage, and neuronal damage. Homocysteine can trigger the release of excitatory amino acids and catecholamines, which may exacerbate neurological conditions. Hyperhomocysteinemia can result from genetic mutations, nutritional deficiencies in folate, vitamin B6, and B12, or environmental factors. It is linked to various cardiovascular and neurological conditions, including hypertension, stroke, and dementia. The SAM-to-SAH ratio, a key indicator of methylation potential, is reduced in hyperhomocysteinemia, leading to decreased methylation and DNA hypomethylation, which can affect gene expression and contribute to disease progression. Homocysteine also influences vascular stiffness and arterial structure, increasing the risk of atherosclerosis and cardiovascular events. Studies show a correlation between elevated homocysteine levels and increased cardiovascular risk, although the exact mechanisms and the extent of its role as a risk factor remain debated. While some research suggests homocysteine is an independent risk factor for CVD, others indicate that its association may be influenced by other factors such as blood pressure and vascular reactivity. Despite these findings, homocysteine is not yet classified as a standard risk factor for CVD in clinical guidelines. However, its potential as a biomarker for cardiovascular disease risk is being explored. Further research is needed to clarify the role of homocysteine in CVD and to determine its utility in risk prediction and management. Nutritional interventions, such as folate and B vitamin supplementation, may help lower homocysteine levels, but their effectiveness in preventing CVD remains a topic of ongoing investigation.