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Heavy Metal Detoxification

General Background

The term “heavy metal” assumes a variety of different meanings throughout the different branches of science. Although “heavy metal” lacks a consistent definition in medical and scientific literature, the term is commonly used to describe the group of dense metals or their related compounds, usually associated with environmental pollution or toxicity (Duffus 2002). Elements fitting this description include lead, mercury, and cadmium. The rather broad definition of heavy metals may also be applied to toxic metalloids (a chemical element that has properties that include a mixture of those of metals and non-metals), like arsenic, as well as nutritionally-essential trace minerals with potential toxicities at elevated intake or exposure (eg, iron, zinc, or copper) (Duffus 2002; Bronstein 2012). 

Although “heavy metal” toxicities due to lead, mercury, and cadmium are generally considered rare in mainstream medicine, less well-recognized is that chronic accumulation that may not achieve classical acute toxicity thresholds may nevertheless contribute to adverse health effects.

Regarding acute toxicity, according to the 2011 National Poison Data System annual report, there were 7337 reported unintentional heavy metal exposures in the United States, resulting in 26 serious health outcomes and 2 deaths (Bronstein 2012). While data from the National Health and Nutrition Examination Survey (NHANES) shows a decade of encouraging year-over-year decreases in acutely toxic heavy metal exposure in the United States, there are still a significant number of people with blood levels that may put them at risk for chronic accumulation, and therefore toxicity, over time (CDC 2013a). For example, in the United States, children are exposed to lead in at least 4 million households. Children are particularly sensitive to lead intoxication, both acute and chronic, and there is no identified safe level of lead exposure in children (CDC 2013b; Koller 2004; Handler 2012; CDC 2012). Further, pregnant women risk toxic exposure to the developing fetus since the mobilization of stored lead from the mother’s bones can leach into the bloodstream, and this is more likely the result of chronic rather than acute lead exposure in the mother (Miranda 2010). With several toxic metals lacking robust pathways for elimination or otherwise remaining in the body for a long time, body burdens of some toxic metals (eg, lead, mercury, cadmium) may increase with age (Bjermo 2013).

While a specific toxic metal has the potential to exert detrimental effects by select mechanisms, there are several common features among toxic heavy metals. One of the most widely studied mechanisms of action for toxic metals is oxidative damage due to direct generation of free radical species and depletion of antioxidant reserves (Ercal 2001). Mercury, cadmium, and lead, for example, can effectively inhibit cellular glutathione peroxidase, reducing the effectiveness of this antioxidant defense system for detoxification (Reddy 1981). Many toxic heavy metals act as molecular “mimics” of nutritionally essential trace elements; as a result, they may compete with essential metallic cofactors for entry into cells and incorporation into enzymes (Jang 2011). For example, cadmium can compete with and displace zinc from proteins and enzymes; lead is chemically similar to calcium; and thallium is a potassium mimic in nerves and the cardiovascular system (Buchko 2000; Jang 2011; Thévenod 2013).​​