The Role of Mercury Toxicity in Hypertension, Cardiovascular Disease and Stroke

The_Journal_of_Clinical_Hypertension2Houston, M. C. (2011), Role of Mercury Toxicity in Hypertension, Cardiovascular Disease, and Stroke. The Journal of Clinical Hypertension, 13: 621–627

Mercury induces mitochondrial dysfunction with reduction in adenosine triphosphate, depletion of glutathione, and increased lipid peroxidation. 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, myocardial infarction, cardiac arrhythmias, reduced heart rate variability, increased carotid intima-media thickness and carotid artery obstruction, cerebrovascular accident, 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 inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to mercury-induced heavy metal toxicity.

Mercury toxicity should be evaluated in any patient with hypertension, coronary heart disease, cerebral vascular disease, cerebrovascular accident, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be performed.


Mercury is the most dangerous of all the heavy metals. It will modify the distribution and retention of other heavy metals. Mercury has no known physiologic role in human metabolism, and the human body has no mechanisms to actively excrete mercury. Mercury thus accumulates during life so that the average 165-lb person has a total body burden of about 13 mg of mercury.

Mercury has a high affinity for sulfhydryl groups, various enzymes and amino acids, N-acetyl cysteine (NAC), alpha lipoic acid (ALA), and glutathione (GSH), which provide about 10% to 50% of the plasma protein antioxidant capacity.8,12,13 Both NAC and ALA, as well as cysteine, are precursors for glutathione, which is the most potent intracellular antioxidant and protects against oxidative stress, inflammation, and cardiovascular disease.3,4,5,8,9,12

This mercury-induced reduction in oxidant defense and increase in oxidative stress increase the risk for CVD and CVA. Selenium antagonizes some of the adverse effects of mercury by forming a seleno-mercury complex in tissue that is less toxic.9,14–20 Higher intake of selenium reduces mercury-related CVD and CVA.


Mercury induces mitochondrial dysfunction and oxidative stress.

The primary three sources of mercury-induced lipid peroxidation include the Fenton reaction, affinity for sulfhydryl groups, and selenium deficiency.

TABLE II. Vascular Biologic Effects of Mercury

1. Increased free radical production and increase in oxidative stress

2. Inactivation of antioxidant defenses

3. Mitochondrial dysfunction

4. Binds to thiol-containing molecules (sulfhydryl groups)

5. Binds to SE forming Se-Hg complex-mercury selenide, which decreases Se available for cofactor with glutathione peroxidase

6. Inactivates glutathione, catalase, superoxide dismutase

7. Increases lipid peroxidation in all organs

8. Increases oxidation of low-density lipoprotein and oxidation of low-density lipoprotein immune complexes

9. Increased platelet aggregation and thrombosis

10. Increased coagulation and thrombosis: increases Factor VIII, platelet factor 4, and thrombin and reduces protein C

11. Inhibit endothelial cell formation and migration and decreases endothelial repair

12. Decreases nitric oxide bioavailability

13. Endothelial dysfunction

14. Increase apoptosis

15. Reduced monocyte function and phagocytosis

16. Immune function is impaired

17. Increased vascular inflammation with increase tumor necrosis factor a and interleukin 6

18. Stimulation of vascular smooth muscle cells

19. Inactivation of paroxonase and other high-density lipoprotein proteins and enzymes

20. Translocaion of membrane phosphytidyl serine

21. Activates phospholipase A2

22. Activates phospholipase D

TABLE III. Summary of the Overall Vascular Biologic Effects of Mercury

1. Oxidative stress

2. Inflammation

3. Thrombosis

4. Vascular smooth muscle proliferation and migration

5. Endothelial dysfunction

6. Dyslipidemia (oxidation of high-density lipoprotein and paraxonase)

7. Immune dysfunction

8. Mitochondrial dysfunction

In summary, the overall vascular effects of mercury include oxidative stress–decreased oxidative defense, inflammation, thrombosis, VSM proliferation and migration, endothelial dysfunction, reduced NO bioavailability, dyslipidemia, immune dysfunction, and mitochondrial dysfunction (Table III). All of these abnormalities have the potential to increase the risk for hypertension, CVD, and CVA.


The clinical consequences of mercury toxicity include hypertension, CHD, MI, reduction in heart rate variability, increase in carotid intima-media thickness (IMT) and carotid obstruction, CVA, generalized atherosclerosis, renal dysfunction, and proteinuria, and an overall increase in total and cardiovascular mortality.

Evidence from these and other epidemiologic and clinical studies suggest that people with high levels of urine, hair, blood, and toenail mercury have an increased risk of cardiovascular diseases.


This important study concluded that there exists a positive monotonic increase in the risk of MI with mercury toenail content above the 0.25 lg ⁄ g level, which was even steeper when adjusted for the DHA adipose tissue content.


Mercury has a high affinity for sulfydryl groups, which inactivate numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (NAC, ALA, GSH) with decreased oxidant defense and increased oxidative stress.

Mercury binds to metallothionein and substitute for zinc, copper, and other trace metals, reducing the effectiveness of metalloenzymes.

Mercury also induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation. Oxidative stress and decreased oxidative defense are common (especially with mercury).

Selenium and fish high in omega-3 fatty acid content antagonize mercury toxicity.

The overall vascular effects of mercury include increases in oxidative stress and inflammation, reduction in oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction.

The clinical consequences of mercury toxicity include hypertension, CHD, MI, cardiac arrhythmias, sudden death, reduced heart rate variability, increased carotid IMT and carotid artery obstruction, 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 inactivates catecholamine-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase BP and may be a clinical clue to mercury toxicity.

Mercury toxicity should be evaluated in any patient with hypertension, CVD, CHD, CVA, or other vascular disease and who have a clinical history of exposure or clinical evidence on examination of mercury overload.

Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be performed. The 24-hour urine measurements should be done with baseline and provoked samples.

Houston, M. C. (2011), Role of Mercury Toxicity in Hypertension, Cardiovascular Disease, and Stroke. The Journal of Clinical Hypertension, 13: 621–627

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About The Author

The Journal of Clinical Hypertension is a peer-reviewed, monthly publication that serves family practitioners, internists, and cardiologists by providing objective, up-to-date information and practical recommendations on the treatment of hypertension. As newer studies are completed, they are summarized and critiqued. Reviews of recent publications in other journals and original papers that focus on the clinical management of hypertension are featured. JCH is the official journal of the American Society of Hypertension

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