Intravenous Chelation Therapy

What is Chelation and How Does it Work

Using chelation therapy for the treatment of heart disease is still considered to be an experimental treatment even though the most recent study showed benefit. Chelation therapy is FDA only approved for toxic metal poisoning and hypercalcemia (a condition of too much calcium). Chelation literally means “to chemically bind to.” Chelation can be administered either orally or intravenously but oral bioavailability is poor.

Chelation may help but this depends on many factors.  I have noticed that it is most effective when elevated levels of reactive metals are present. Several theories have been proposed for how this treatment may work. One theory suggests that EDTA chelation might work by directly removing calcium found in fatty plaques that block the arteries, causing the plaque to decrease in volume.

Another is that the process of chelation may stimulate the release of a hormone (calcitonin) that in turn causes calcium to be removed from the plaques and redistributed. A third theory is that chelation therapy may work by reducing the damaging effects of oxygen ions and reactive transition metals (oxidative stress) on the walls of the blood vessels. Reducing oxidative stress could reduce inflammation in the arteries and improve blood vessel function. This is why EDTA is used to prevent the spoiling of food. It blocks oxidative reactions.

The ability of EDTA to neutralize oxidative reactions caused by transition metals (Lamb, Mitchinson, & Leake, 1995; Stadler, Lindner, & Davies, 2004) has many beneficial anti aging effects on the body. Transition metals are those in the middle of the periodic table.  Transition metals/minerals can form negatively charged complexes that are reactive. Most toxic metals (minerals) are transition metals as well as the nutritionally essential metals iron and copper.

LDL oxidation can only take place in the presence of transition metal ions, such as iron and copper and human plaque biopsies contain significant amounts of reactive copper and iron  (Lamb, et al., 1995; Stadler, et al., 2004) whereas the blood usually does not contain these highly reactive species (Lamb, et al., 1995).

Giving more credibility to the notion that chelation is a valid treatment is published data indicating that heavy metals, particularly mercury, may contribute to atherosclerosis (Landmark & Aursnes, 2004). The negative cardiovascular effects of mercury stem from its ability to induce oxidative stress, inflammation, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, immune dysfunction, and mitochondrial dysfunction (Houston, 2007).

Lead is very bad for the cardiovascular system as well. The main sources of lead exposure are lead-based paint, leaded gasoline, lead-soldered plumbing fixtures, pipes, and canned foods, contaminated alcoholic beverages, lead-glazed kitchen/dining utensils, and mining and industrial contaminations, as well as occupational exposure. Since the banning of lead-based gasoline, paint, and solder, as well as passage and enforcement of environmental regulations, exposure to lead in the U.S. has declined. Ground contamination continues to be a current source of lead exposure in the industrial societies. Heavy exposure also continues in countries where environmental regulations are lax or poorly enforced (such as India and China) (Vaziri, 2008). Keep in mind the U.S. had no regulations either roughly prior to 1960.

Lead can be absorbed via the respiratory and gastrointestinal tracts and even through the skin. Over 95% of the total body lead content resides in the bone, where it can persist for decades. As we age gradual release of lead from the bone serves as a source of toxicity long after initial exposure.  Conditions such as osteoporosis accelerate the release of lead from bone. Measurement of blood lead concentration primarily reflects recent/current lead exposure and does not reveal past exposure. Measurement of urinary lead excretion after EDTA provocation provides the best estimation of total body lead burden (Vaziri, 2008).

The negative effects of lead on the cardiovascular system are really quite impressive. Chronic lead exposure causes high blood pressure, tyhrombosis and cardiovascular disease by (Vaziri, 2008):
1. promoting oxidative stress
2. limiting nitric oxide availability
3. impairing nitric oxide signaling
4. augmenting adrenergic activity
5. increasing endothelin production
6. altering the renin-angiotensin system
7. raising vasoconstrictor prostaglandins
8. lowering vasodilator prostaglandins
9. promoting inflammation
10. disturbing vascular smooth muscle Ca2+ signaling
11. diminishing endothelium-dependent vasorelaxation
12. causing endothelial injury and limiting endothelial and blood vessel repair
13.  inhibiting angiogenesis
14.  reduce endothelial cell growth
15.  reducing tissue plasminogen activator and raising plasminogen activator inhibitor-1 production

The fact that heavy metals cause oxidative stress and cardiovascular disease is undisputed in the literature (Valko, Morris, & Cronin, 2005; Wolf & Baynes, 2007). Critics of chelation conveniently fail to mention or look at this data. Because of the connection between heavy metals in atherosclerosis I will often screen patients for toxic metal overload and only recommend chelation for the treatment of heavy metal toxicity. Anyone who has high blood pressure and atherosclerosis should be screened for toxic metals with a urinary provocation test.