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.
Mercury inactivates catecholaminei-0-methyl transferase (COMT). COMT is an enzyme principally involved in catabolism (the breaking down) of catecholamines at the sympathetic nerve endings.
Catecholamines are hormones made by the adrenal glands. These glands are on top of the kidneys. Catecholamines are released into the blood when a person is under physical or emotional stress. The main catecholamines are dopamine, norepinephrine, and epinephrine (which used to be called adrenalin).
The consequence of mercury on COMT is the fact that serum and urinary epinephrine, norepinephrine, and dopamine will increase. This effect will increase blood pressure and may be a clinical clue to mercury-induced heavy metal toxicity.
It is important to note that mercury diminishes the protective effect of fish and omega-3 fatty acids which has been found to have value in the management of reducing high blood pressure.
Mercury toxicity should be evaluated in any patient with hypertension, coronary heart disease, cerebral vascular disease, cerebrovascular accident, or other vascular disease.
If you are suffering with hypertension it is of vital importance to have your doctor order the following labs: Erythrocyte and whole blood toxic element levels and/or a 24 hour toxic metal urine tests using a challenging chelating agent like DMSA.
If your test reveals high levels of mercury it is important to find a doctor trained in functional medicine and is able to prescribe an effective protocol to chelate the toxic metal and decrease the load on your body.
This in fact may be the missing piece of the puzzle in reducing high blood pressure.
Houston MC, Role of mercury toxicity in hypertension, cardiovascular disease, and stroke.J Clin Hypertens (Greenwich). 2011 Aug;13(8):621-7.
The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of Dr. Grisanti and his functional medicine community. Dr. Grisanti encourages you to make your own health care decisions based upon your research and in partnership with a qualified health care professional. Visit www.FunctionalMedicineUniversity.com to find practitioners thoroughly trained in functional medicine. Look for practitioners who have successfully completed the Functional Medicine University's Certification Program (CFMP).
Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., M.S.
Michael Jurgelewicz, DC, DACBN, DCBCN
Psoriasis is an inflammatory skin condition that is characterized by itchy, scaly skin plaques. The exact cause of psoriasis is unknown; however, more and more evidence suggests that the immune system can be a culprit when it is chronically stimulated, causing an overproduction of cytokines, which maintains an inflammatory environment.
According to a new study published in the journal International Immunology, researchers have discovered more evidence that a cytokine called IL-17A is especially critical in the pathogenesis of psoriasis.
In this study, researchers cultured normal keratinocytes with a mixture of six different cytokines known to be involved in psoriasis and, as a result, found that this caused the expression of psoriasis-related genes. The research team identified a group of psoriasis-related genes in keratinocytes that are regulated by IL-17A. One of these genes in particular, called NFKBIZ, was found to have a significant role in the IL-17A pathway. This gene encodes a protein that plays a well-known role in regulating the body's immune response to infection.
What appears to happen with most autoimmune conditions is that there are multiple triggers chronically stimulating the immune system over a long period of time in multiple ways. As a result, the immune system goes into an overloaded, overwhelmed state and loses its ability to function.
If we know what causes the immune system to attack itself and we know some of the triggers that cause a malfunction in the immune system, we can then strive to successfully treat these conditions.
There are various autoimmune diseases within all specialties, and all of these are looked at differently. Nevertheless, they all have the same common triggers. Therefore, we can take a similar approach in working with all autoimmune conditions.
Nutrients to Consider
There are only a few natural products that have demonstrated such a wide range of protective properties as those containing curcumin. This powerful component of the Indian spice turmeric provides anti-inflammatory properties and antioxidant effects that modulate cytokine and chemokine production, and as a result balances the Th-1 and Th-2 T helper cells further downstream.
Glucosamine is a derivative of glucose which can be converted in cells to N-acetyl glucosamine (GlcNAc). This novel form of glucosamine has demonstrated that it acts as an immunosuppressive agent through a variety of mechanisms. Glucosamine can suppress the activation of T-cells and dendritic cells, both being critically involved in the immune response. In one study, when GlcNAc was used in children with chronic inflammatory bowel disease, biopsies revealed histological improvements as well as restoration of the epithelial barrier (i.e., repairing leaky gut).
ParActin® is a branded botanical that has very unique immune-modulating properties. It is a standardized, special extract of Andrographis. In low doses (25-30mg) it actually acts as an immune stimulant, but at higher doses (150-500mg) it activates the peroxisome proliferator activated receptor gamma (PPARγ) nuclear receptor. When activated, it stimulates the expression of genes involved in energy homeostasis as well as key regulators of the immune and inflammatory responses.
Muromoto R, Hirao T, Tawa K, Hirashima K, Kon S, Kitai Y, Matsuda T. IL-17A plays a central role in the expression of psoriasis signature genes through the induction of IκB-ζ in keratinocytes. International Immunology. March 3, 2016.
Ronald Grisanti D.C., D.A.B.C.O.,D.A.C.B.N., M.S.
Darkening of the skin at the nape of the neck could be an early indication of insulin resistance and diabetes.
The condition, called Acanthosis Nigricans (AN), is marked by the darkening and thickening of the skin on the sides or back of the neck, the armpits, under the breast, and groin.
Acanthosis Nigricans is a skin condition that signals high insulin levels in the body.
Acanthosis Nigricans is important because these markings can help identify persons who run the risk of developing diabetes in the future.
Once identified, the necessary measures to lower the insulin levels and reduce the risk of developing diabetes can be taken.
Similarly, the acanthosis nigricans markers will begin to fade.
Acanthosis nigricans is a skin manifestation of insulin resistance and an early indication of diabetes," says Dr Anoop Misra, professor of medicine at the All India Institute of Medical Sciences (AIIMS), New Delhi.
Dr. Misra's study followed adult patients with acanthosis nigricans who had no history of diabetes and discover that 58% of the patients reviewed had the metabolic syndrome. In fact 24% had full-blown diabetes.
All were clueless about their diabetic status.
Who is Dr. Anoop Misra?
Dr Misra is considered as a lead researcher internationally for insulin resistance, diabetes mellitus, hyperlipidemia and obesity in the Indian population. He has substantially contributed to the understanding of the mechanisms, prevention and management of obesity and diabetes mellitus in Indians by publishing more than 100 papers in the international journals, and debating on important issues in the International conferences.He has worked as the World Health Organization fellow at Royal Free Medical School, London and University of Texas Southwestern Medical Center at Dallas. He also worked as faculty in Internal Medicine and Endocrinology at the prestigious University of Texas Southwestern Medical Center at Dallas.
Reinehr T. Clinical presentation of type 2 diabetes mellitus in children and adolescents. Int J Obes (Lond). 2005 Sep;29 Suppl 2:S105-10.
Charnvises K, Weerakiet S, Tingthanatikul Y, Wansumrith S, Chanprasertyothin S, Rojanasakul A. Acanthosis nigricans: clinical predictor of abnormal glucose tolerance in Asian women with polycystic ovary syndrome. Gynecol Endocrinol. 2005 Sep;21(3):161-4.
Mohrenschlager M, Ring J, Kohn FM.Diabetes mellitus: [Cutaneous and mucosal marker lesions] MMW Fortschr Med. 2005 Oct 6;147(40):34-6.
Bolding J, Wratchford T, Perkins K, Ogershok P.Prevalence of obesity, acanthosis nigricans and hyperinsulinemia in an adolescent clinic. W V Med J. 2005 May-Jun;101(3):112-5.
Grandhe NP, Bhansali A, Dogra S, Kumar B.Acanthosis nigricans: relation with type 2 diabetes mellitus, anthropometric variables, and body mass in Indians.
Postgrad Med J. 2005 Aug;81(958):541-4.
Flagothier C, Quatresooz P, Bourguignon R, Pierard-Franchimont C, Pierard GE. Abstract [Cutaneous stigmata of diabetes mellitus] Rev Med Liege. 2005 May-Jun;60(5-6):553-9.
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