Heavy Metals Play a Huge Role in Diseases and Aging

New Scientific Research Proves Ca-EDTA Benefits with Detoxamin

Now, a burst of papers recently published in prestigious journals finally confirms that low levels of heavy metals---even at levels that were once considered "safe"---are in fact, most definitely dangerous.

This new research documents the effects of these toxic metals as they accumulate in the body over time, and clearly indicates that Ca-EDTA chelation therapy provides benefits by reducing the body's burden of these toxic heavy metals, resulting in improved physiological functioning and much better health.

Lead Increases Cancer, Vascular Disease, and Overall Mortality

Lead poisoning has long been recognized as a health hazard. Lead has been historically used in a number of industrial processes, including manufacturing batteries, paints, and adding it to gasoline. Acute (high exposure) lead poisoning causes symptoms of abdominal pain or "lead colic" cognitive deficits, peripheral neuropathy, arthralgias, decreased libido, and anemia.

Lead is practically everywhere in today's environment. It enters our bodies from many sources including defective glazes (pottery), drinking water, contaminated soil, airborne particulate, leaded gasoline, paint and several other sources. Symptoms of lead poisoning are stomach pains, constipation, diarrhea, aggressiveness, anxiousness, hyperactivity, muscle pain, weakness, weight loss, learning disabilities, convulsions and eventual death with chronic lead poisoning.

Lead poisoning victims usually become anemic. These symptoms usually persist for about 2 weeks from time of exposure, and then settle into the organs, bones & even hair.

Unfortunately, we still do not know the long-term effects of lead exposure. Long-term exposure to low levels of lead may result in the gradual accumulation of lead and the development of many disorders and different diseases like learning and behavior problems, kidney and cardiovascular diseases, decreased fertility, cancer and hypertension.1


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Drs. Mark Lustberg, of the University of Maryland School of Medicine, and Ellen Silbergeld recently compared data from the 2000 U.S. census and the huge Third National Health and Nutrition Examination Survey (NHANES-III). 2 Lustberg and Silbergeld concluded that an estimated 29 million people (15% of the adult population over the age of 20) had blood lead levels (BLL) of at least 20 mcg/dL from 1976-1980, and presently a minimum of 1.7 million people in the US have BLL of at least 20 mcg/dL.

The authors then examined the death rates of the participants in the NHANE Survey with low levels of lead-people who had less than 30 mcg per dL (30 mcg per dL is the level normally considered "toxic"). They found that BLL's ranging from as little as 20 to 29 mcg per dL were associated with a 39% increase in mortality from all causes. These "low" levels of lead were also linked with a 46 percent increase in mortality from cardiovascular diseases, and a whopping 68 percent increase in mortality due to cancer.

Even lower BLL's that measured from 10 to 19 mcg/dL were associated with a significant 17 percent increase in mortality from all causes and a 46 percent increase in cancer.

The heavy metals most often linked to human poisoning are lead, mercury, aluminum, arsenic, nickel and cadmium. Other heavy metals, including copper, and zinc are required by the body in small amounts, but can be toxic in larger doses. Sources of heavy metals in the environment include air emissions from coal-burning plants, smelters, and other industrial facilities; waste incinerators; process wastes from mining and industry; and lead in household plumbing and old house paints. While certain types of industrial facilities are required by the EPA to report their releases of some heavy metals to the Toxics Release Inventory (TRI), other major sources - including power plants and waste incinerators - are not. Consequently, the TRI may significantly under-report actual environmental releases of some metals.

Heavy metals can also enter the environment through natural processes. For example, in some parts of the U.S., naturally occurring geologic deposits of arsenic dissolve into groundwater, potentially resulting in unsafe levels of this metal in drinking water supplies. Once released to the environment, metals can remain for decades or centuries, increasing the likelihood of human exposure.

Humans are exposed to heavy metals through inhalation of air pollutants, consumption of contaminated drinking water, exposure to contaminated soils or industrial waste, or consumption of contaminated food. Food sources such as vegetables, grains, fruits, fish and shellfish can become contaminated by accumulating metals from surrounding soil and water. Heavy metals cause serious health effects, including reduced growth and development, cancer, organ damage, nervous system damage, and in extreme cases, death. Exposure to some metals, such as mercury and lead, may also cause development of autoimmunity, in which a person's immune system attacks its own cells. This can lead to joint diseases such as rheumatoid arthritis, and diseases of the kidneys, circulatory system, and nervous system.

Metals are particularly toxic to the sensitive, rapidly developing systems of the fetus, infants and young children. Some metals, such as lead and mercury, easily cross the placenta and damage the fetal brain. Childhood exposure to some metals can result in learning difficulties, memory impairment, damage to the nervous system, and behavioral problems such as aggressiveness and hyperactivity. At higher doses, heavy metals can cause irreversible brain damage. Children may receive higher doses of metals from food than adults, since they consume more food for their body weight than adults.

References:

1. Lustberg, Mark and Silbergeld, Ellen. Blood lead levels and mortality. Arch Intern Med, 2002, 162: 2443-2449.

2. Pinkle, J.L., Brody, D.J., Gunter, E.W., et al. The decline in blood lead levels in the United States: the National Health and Nutrition Examination Surveys (NHANES). JAMA, 1994, 272: 284-291


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