Homocysteine and Nighttime Blood Pressure Dipping—Is There a Connection?

Increased plasma level of homocysteine is a risk factor for neural tube defects and has been associated with many noncommunicable diseases, including cardiovascular and cerebrovascular diseases, type 2 diabetes, and cancer.^1–3 Homocysteine is a major independent biomarker for endothelial dysfunction, as it leads to an imbalance between blood endothelin-1 and nitric oxide levels, affects the proliferation of smooth muscle cells, and induces subclinical inflammation—thereby contributing to increased vascular endothelial damage and atherosclerosis in clinical patients.⁴ The role of homocysteine in endothelial dysfunction is thought to be mediated by mechanisms including oxidative stress, nuclear factor-kb activation, inflammation, and inhibition of endothelial nitric oxide synthase.⁵ It is also well documented that homocysteine is capable of triggering neuronal damage via oxidative stress, and may exert several functions as potential neurotransmitter.⁴ The contribution of homocysteine toward sympathetic nervous system activation is still controversial with animal studies suggesting that acute homocysteine administration does not lead to sympathetic activation,⁶ whereas others found that hyperhomocysteinemia did induce dysfunction of the autonomic system.⁷

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