The role of mercury and cadmium in cardiovascular disease, hypertension, and stroke

Abstract

Mercury and cadmium have a high affinity for sulfhydryl (-SH) groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (NAC, ALA, and GSH), with subsequent decreased oxidant defense and increased oxidative stress. Both bind to metallothionein and substitute for zinc, copper, and other trace metals reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation. An increased oxidative stress and reduced oxidative defense are common. Selenium and fish containing omega 3 fatty acids antagonize mercury toxicity. The overall vascular effects of mercury include increased oxidative stress and inflammation, reduced oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, coronary heart disease (CHD), myocardial infarction (MI), cardiac arrhythmias, reduced heart rate variability (HRV), increased carotid intimal medial thickness (IMT) and carotid artery obstruction, cerebrovascular accidents (CVA), generalized atherosclerosis, and renal dysfunction, insufficiency, and proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury and cadmium inactivate catecholamine-O-methyl transferase (COMT), which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to heavy metal toxicity. Cadmium concentrates specifically in the kidney, inducing proteinuria, renal dysfunction, and insufficiency. Cadmium is associated with hypertension, but less so with CHD, CVD, and CVA. Renal cadmium reduces CYP4A11 and PPARs, which may be related to hypertension, sodium retention, glucose intolerance, dyslipidemia, and zinc deficiency. Dietary calcium may mitigate some of the toxicity of cadmium. Mercury and cadmium heavy metal toxicity should be evaluated in any patient with hypertension, CHD, CVD, CVA, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be done.