Month: February 2016

Three Chelation Physicians respond to the TACT I results

 “IMPORTANT NEWS FLASH FOR NATURAL MEDICINE”  Robban Sica MD

This week the long awaited results of a seven year research trial, known as the TACT trial, were finally released demonstrating a significant positive result of chelation therapy in the treatment of cardiovascular disease and prevention of negative outcomes of this disease such as stroke, heart attack, amputation and death. TACT, which is the Trial to Assess Chelation Therapy, called on the expertise of university cardiologists and experienced chelation physicians from around the United States. The objective of the study centered on comparisons between patients with significant cardiovascular disease, who were treated with medication and intravenous chelation therapy to those receiving medication but no chelation. The results indicated significant improvement in patients with previous heart attacks who were already under cardiology treatment- especially patients with diabetes. The group treated with chelation had fewer subsequent surgeries than those who received a placebo. In addition, findings show chelation reduced death from heart attacks by 18% and over 39% for diabetics. Although, some among conventional cardiologists have already attempted to discredit this large and well-controlled trial sponsored by the National Institutes of Health (NIH) Heart, Lung & Blood Institute as well as the National Center for Complementary & Alternative Medicine, the results speak for themselves, especially in diabetics who are at extremely high risk for vascular diseases.

I have been administering the IV treatment since 1989 in my office and have personally observed remarkable improvements in many of my patients receiving chelation therapy, both for heavy metal detoxification and for heart and vascular conditions. As a result, I have been an advocate of chelation therapy for many years. Please call or contact us for more information.

 “LifeForce Newsletter on TACT”  John Parks Trowbridge MD

The take-home message: we do chelation very, very well – just come by anytime to talk with our patients and learn first-hand of their stunning successes. The NIH researchers just reported – at the American Heart Association meeting – that there were slightly fewer heart attacks (and deaths) and slightly fewer bypass operations and stents in the treated group. If this were a NEW drug, they would have reported on its stunning potential to reduce heart attacks. That’s because it’s easy to “lie” with how you interpret statistics.

But since the very beginning, I’ve said that the final report would be something like: “Review of the clinical experience suggests that chelation treatments might provide a small but encouraging benefit to a select group of patients. Further studies will be needed to determine whether this effect is real and also worthwhile.”

And that, my friends, is pretty much exactly what the report concluded! (How did I know? Could 29+ years of debating with “regular docs” have given me the idea that they really don’t want to acknowledge any improvements with chelation?) Diabetics got the best results. For those of you who don’t know, I’ve taught chelation extensively since 1984. I’ve written several books, articles, CDs, and DVDs (even an audiobook) on chelation – all available from our office, just DIAL 1-800-FIX-PAIN. I’ve lectured on chelation in Taiwan and Brazil. I’ve served for years on the board of our specialty organization – the American Board of Clinical Metal Toxicology – where I was certified as one of the first specialists in 1985.

Most importantly, I’ve been blessed to watch thousands of patients show dramatic improvements with their chelation treatment programs – saving limbs from amputation, reducing insulin dosages, improving physical performance, even helping mental clarity and depression. Have we been reducing heart attacks and strokes along with amputations? The list goes on and on. What was WRONG with the NIH study, that they didn’t see such dramatic results? Sadly, they offered only 40 treatments and NO “monthly boosters.” Their “multi-vitamin” dosages were smaller than ours. We focus on adjusting treatments to remove toxic metals (by using a variety of personalized FDA-approved medications), because our experience and studies show that these heavy metals (lead, mercury, arsenic, cadmium, and so on) are directly related to inflammation and degenerative diseases, early aging, disability and death. And, of course, our iv treatment solution (which is customized for each patient) and nutritional support programs (also customized) are much more complex than the basic ones used in the study. (I do have a Master’s degree in nutrition as well as my M.D. degree and training.) The list is longer – but also boring.

The take-home message: we do chelation very, very well – just come by anytime to talk with our patients and learn first-hand of their stunning successes. (Or are you going to be one of the many who waits til some calamity occurs … and then jump on the “medical merry-go-round”? Which choice does your family deserve?)

 “My Impressions and Response to the Trial to Assess Chelation Therapy Recently Completed by the NIH” Conrad Maulfair DO

Chelation Therapy is a wonderfully effective, safe, comprehensive program that can benefit people with chronic degenerative diseases.  People with conditions like heart disease, diabetes, arthritis, lack of energy and problems of aging can experience a resurgence of energy and life quality.  This program is not new.  It has been studied and offered to patients by many progressive physicians to hundreds of thousands of thankful people world wide for over 60 years.  Patients who receive chelation therapy experience their quality of life improve first hand.  The doctors who provide individualized programs enjoy their observations of their patients’ improvements.

It makes our day that we are no longer alone in these observations; the United States government via the National Institutes of Health (NIH) funded a study on chelation therapy.  The study called TACT, Trial to Assess Chelation Therapy, started in 2003.  The results were just announced at the American Heart Association’s meeting November 4, 2012.  The results were positive.

People in this trial who received Chelation Therapy had decreased hospitalizations for angina, compared to the control group.  There were fewer deaths from heart attacks and strokes for the patients receiving chelation therapy.  The chelation patients also needed less bypass surgeries and angioplasties; the findings were especially positive for patients who also suffered from diabetes.  Chelation Therapy reduced cardiac events by 18% and by 39% for diabetic patients.  The total reduction in cardiac events was statistically significant.  Physicians conducting the study included university cardiologists and experienced chelation physicians.

Keep in mind  all study participants had a previous heart problem before beginning the trial, 83% had either bypass surgeries, angioplasty with or without stents. The majority of participants had high blood pressure and 73% had been prescribed cholesterol lowering statin drugs.  One thousand seven hundred people participated in the study.  An additional finding was the unquestionable safety of Chelation Therapy.

Considering the decrease need for angioplasty and bypass surgery would you be surprised to see the cardiology and cardiovascular surgeons less than enthusiastic about the study results?

Those of us who have been trained to provide Chelation Therapy for the benefit of our patients have known for many years the wide range of improvement possible for our patients.  Through thick and thin our care has been without support in the main from mainstream medicos, so we welcome the scientific evidence from a large clinical trial that confirms some of the many benefits we have observed in our patients.

Truth be told, however, if the study was not positive I would have continued to provide Chelation Therapy to my patient family and continued my own Chelation program.  I know the benefits of providing Chelation Therapy after forty years of providing this care in clinical practice.  I see PVD, heart disease, high blood pressure, and diabetes abate all the time.  Some of our diabetic patients no longer require insulin injections.

I am willing to talk with any sincere person about any aspect of this study.  I welcome your questions.

 

Magnesium deficiency or composition of the infusate used in the load test?

Robert Waters MD

ABSTRACT

Mg Man Cal tiss-04-17-08

Serum/plasma measurements do not reflect magnesium deficits in clinical situations and magnesium load tests are used as a more accurate method to identify magnesium deficiency in a variety of disease states as well as in subclinical conditions. The objective of this study was to determine if people are indeed magnesium deficient or if the apparent magnesium deficiency is due to the composition of the infusate used in the load test.

Magnesium load tests were performed on 7 patients using three different Mg solution infusions- a Mg-EDTA (ethylene diamine tetraacetic acid)-nutrient cocktail used in EDTA chelation therapy containing several components including vitamins and minerals and the same cocktail without EDTA and an infusion of an identical amount of magnesium in normal saline solution.  There was no significant difference in the amount of magnesium retained in the 24 hours after infusion among the three infusates.  All infusates resulted in very high magnesium retention compared to previous published magnesium load studies.  Magnesium deficiency may be widespread and the relationship of Mg deficiency to related diseases requires further study.

INTRODUCTION

Mg is the fourth most abundant cation in the body and its intracellular concentration is exceeded only by potassium [1].  Mg activates more than 300 enzymes in the human body [2].  Deficiency of Mg has been linked to a variety of clinical disease states including hypertension, myocardial infarction, cardiac dysrhythmias, coronary spasm and premature artherosclerosis [3].  In addition, patients with diabetes have been found to be at particular risk for Mg deficiency [4].  Conditions related to the deficiency of Mg may be linked to its functions as a cofactor for enzymes related to cell respiration, glycolysis and ion transport (e.g. Na-K-ATPase).  In fact, the central position of Mg in its role in energy storage, transfer and utilization is mediated through its function in the formation of Mg-ATP, the ultimate form of stored energy in biological systems.  In addition, Mg has functions related to protein synthesis through its action on nucleic acid polymerization, binding of ribosomes to RNA and the synthesis and degradation of DNA [5].  Mg is also an integral player in calcium biology via its ability to maintain low resting concentrations of intracellular calcium ions.  It competes with calcium for membrane binding sites and as such has been described as a “calcium channel blocker” [6].

In degenerative diseases, Mg deficiency has been shown to be related to the generation of free radicals [7].  Mg deficiency has also been shown to negatively influence the generation of nitric oxide and therefore the impact of such deficiency may be responsible in part for the pathogenesis of endothelial dysfunction and its relationship to vascular disease, diabetes and other diseases associated with aging [8].

In a previous study, we showed that after the infusion of 686 mg of elemental Mg as Mg sulfate, in an EDTA chelation “cocktail”, 83% of the infused Mg was retained in the initial 24 hours following infusion [9]. This degree of retention of Mg has generally been recognized to represent evidence of severe Mg deficiency.  However, in that study, it was not clear if the apparent Mg retention was due to a true Mg deficiency or if the components of the chelation cocktail affected Mg retention.  Guldager et al. [10] infused 3 g of EDTA in saline, without any Mg, into a group of peripheral vascular disease patients and collected 24 hour urines of the patients and controls.  There was a highly significant decrease in the Mg in the 24 hour urines of the EDTA patients vs the controls indicating that the EDTA increased Mg retention.  The serum Mg in these patients did not increase so it is probable that the EDTA caused Mg to enter intracellular compartments.  This present study was designed to determine the effects of components of the Mg infusates on Mg retention.

PATIENTS AND METHODS

The study was approved by the Clinic Human Studies Review Board, Wisconsin Dells, WI.  The study was explained to the subjects and patients signed an informed consent before the study.  Data are available to the participants upon request.  Participants did not incur any medical fees as a result of their participation and were not paid for their participation.

At the onset of the study, patients were instructed in the accurate collection of 24-h urine specimens to avoid metal contamination.  Twenty-four-hour urine samples were collected in 4-L sample containers (Fisher Scientific Co., Pittsburgh, PA) 2d prior to chelation therapy (d 1 and d 2), the day of chelation therapy (d 3), and the following day (d 4).  Control urine samples were collected on Monday and Tuesday and the post-infusion urine samples on Wednesday and Thursday.  In Phase 1 of the study, on Wednesday morning of the study week, an intravenous infusion of 2.25 g of EDTA mixed in sterile water with 5 g of sodium ascorbate, 2500 units of heparin, 3 mL of 2% procaine, 100mg pyridoxine HCl, 4 meq KCl, 1 mL of 8.4% sodium bicarbonate, 1000 µg hydroxycobalamin, 1 mL vitamin B complex, and 7 mL magnesium sulfate equivalent to 686 mg of elemental magnesium was given in an arm vein over a 2.5 hour period. During phase 2, patients received an identical infusion without any EDTA and during phase 3 subjects received 686 mg elemental Mg in saline [9] [11].  Order of the phases was random.  The procedures were two to four weeks apart.  Magnesium contents of the urine samples were measured and the Mg retention calculated using the following formula modified from Jeppesen [12]:

%Mg retention = [infused Mg – (urine Mg on day 3 – average urine Mg on days 1 and 2)/ infused Mg] X 100.

Day 3 was the following day after the infusion; days 1 and 2 were baseline days immediately preceding the infusion. In addition, Mg content was also measured on day 4.

Since the time of our original chelation study, published and anecdotal data have revealed that the clinical efficacy of EDTA chelation therapy could be achieved with a smaller dose of EDTA with fewer potential side effects.  Therefore, we reduced the dose of EDTA to 2.25 g.

Magnesium concentrations in the urine were determined using flame atomic absorption using a Perkin-Elmer 5000 flame atomic absorption spectrometer using standard techniques (Perkin-Elmer, Norwalk, CT) and reference materials as described [13].

Statistics: Statistical analyses of the data were performed using 2-Way Analysis of Variance (SAS Institute, Cary, NC, version 9.1).  The main effects were the variable components of the infusions in the 3 Phases.  Values are mean ±  SEM.

RESULTS

Means for magnesium losses among the three Phases were not statistically different.  Approximately 70% of the infused Mg was retained during the 24-h period after the infusion (day 3) in Phase 1.  Retention of Mg in Phases 2 and 3 were similar.  By day 4, the 24-h Mg excretion was not significantly different from the averages of days 1 and 2 in all three Phases of the study.

DISCUSSION

In this study, Mg retention was greater than 70% for all infusates.  High Mg retention is probably not due components of the infusate since infusion of Mg added to saline also led to significant Mg retention. The presence of EDTA in the cocktail did not increase the retention of Mg and retention was still approximately 72% when Mg sulfate was added to saline alone and infused.  Suboptimal Mg status appears to be present in essentially all of the subjects.

From analyzing the data on Mg load tests published over the last 30 years, it appears that there is great variation in the percentage of Mg that can be expected to be retained by normal patients vs. patients with various medical conditions.  It is clear that serum/plasma Mg measurements do not necessarily reflect Mg deficits in clinical situations [14].  Thus alternative measurements of Mg status were attempted and ultimately the Mg retention test was suggested as a more accurate method to identify Mg deficiency in a variety of disease states as well as in subclinical conditions.  Other methods including bone Mg, muscle Mg, NMR spectroscopy, single ion channel analysis, leukocyte Mg, intraerythrocyte Mg and Mg balance studies are more expensive and/or invasive but may not be more informative than the Mg load test.  Even the intracellular Mg measurements have shown inconsistent correlation with serum levels and other tissue levels as well as Mg load test data [15].

Table 2 summarizes the data from a number of intravenous load tests.  In most of the studies, the demarcation in Mg retention between patients and controls is roughly 20%.  In our present study, all groups of patients had Mg retention of at least 70%.  The presence of EDTA at a dose of 2.25g in the infused Mg preparation did not explain the high retention since when EDTA was omitted from the infusate, Mg retention remained high.  However, we cannot, with certainty, conclude that EDTA results in no greater Mg retention since we only used 2.25g of EDTA in the infusions vs the prior study of 3.0g which resulted in an even greater retention of 83% [9].   The results of Guldagner, et al also suggest a causal Mg retention by 3g of EDTA without any Mg added to the infusate [10].

Components of the infusate in the present study also appear to have little influence on magnesium retention since the Phase 2 Mg retention cocktail without EDTA, but otherwise the same vitamins and minerals, was not different from the cocktail containing only Mg and saline.  Patients in our earlier study [9] all had evidence of degenerative diseases and retained even greater amounts of Mg than the patients in our present study and the dose of EDTA in that study was 3 g. Earlier studies of the therapeutic effects of EDTA used 5 g of EDTA per treatment, 5 days per week, and showed dramatic positive clinical effects as well as objective evidence of benefits such as improved EKG’s, reduction in the calcification of heart valves and dissolution of metastatic calcification in the kidneys [16] [17]. Only further studies on the dose dependent effects of EDTA  as well as careful choice of “normal” vs. “diseased” patients can help resolve the issue of whether EDTA can influence calcium and magnesium dynamics in vivo in correlation with clinical and biochemical findings.

A number of studies using the Mg retention test have shown that patients with corornary heart disease are Mg deficient compared to controls.  Jeppesen reasoned that Greenlanders have a lower rate of myocardial infarction as a result of their high serum Mg, low serum calcium and prolonged bleeding time (known to be induced by Mg administration) [12].   After administering 30 mmoles of intravenous Mg over 12 hours in patients with acute myocardial infarction, the infarction patients retained 42% of the infused Mg over the next 24 hours compared to only 22% in the control group.  He also obtained quadricep muscle biopsies, which revealed an increased Mg content in the control group vs the acute myocardial infarction groups but differences were not statistically significant.

Sjogren et al. [18] showed patients with Crohn’s disease had lower tissue concentrations of Mg compared with controls and after IV infusions of 60 mmole Mg, the Crohn’s patients had significantly higher Mg retention than the controls.  Gullestad et al. [19] showed that Mg retention in the 24 hour urine was 3-4% in a group of individuals without known predisposition for Mg deficiency after an infusion of 30 mmoles Mg sulfate.  This was significantly lower than that for 661 hospitalized patients with known predisposition to Mg deficiency (cardiovascular disease, alcoholism, etc. whose percent retention varied from 16 – 38%).  Interestingly, the serum Mg was similar in the patient groups and the controls except for the alcoholics, hypertensives and young healthy controls who had significantly reduced levels.

This later finding, particularly in reference to “young healthy” controls, brings up the probability that dietary intake of Mg is suboptimal and Western diets may be contributing to an increasing problem of Mg deficiency which may be a component of the growing epidemic of the metabolic syndrome and related diseases.

This possibility is supported by manuscripts of Resnick and associates spanning from 1984  to 2000 [20] [21].  Using Mg-specific selective ion electrode apparatus and 31P-NMR spectroscopy, there was a significant correlation between intracellular ionized Mg as well as intracellular free Mg and the presence of NIDDM [22].  Other studies reported increased intracellular calcium, decreased intracellular Mg and decreased cytosolic pH with the presence of essential hypertension [23].  A 1992 study revealed that oral glucose loading, even in normal subjects, elevates free calcium and suppresses free Mg [24].  These data suggest, in the author’s words, “an ionic hypothesis of cardiovascular and metabolic disease in which a generalized defect in cell ion handling is present in all tissues.”  This trend leads to, in different tissues, the features of the metabolic syndrome, hypertension, obesity, insulin resistance and left ventricular hypertrophy, the latter related both to hypertension and, independently, vasoconstriction and increased contractility caused by high cytosolic calcium and lowered free Mg [24].  Arterial stiffness, as measured by High Frequency Ultrasound analysis, is known to correlate with hypertension and coronary heart disease [25].  Resnick et al. [26] showed, using direct magnetic resonance determination of aortic distensibility, that in essential hypertension, there are statistically significant correlations between fasting glucose, abdominal visceral fat and in situ intracellular Mg.

In a rat model, Barbagallo et al. [27] showed that glucose, at increasing mM concentrations, caused a significant increase in cytosolic free calcium in vascular smooth muscle.  The authors suggest that these cellular effects of hyperglycemia may underlie the predisposition of patients with diabetes and patients with insulin resistance to hypertension and vascular diseases.  The same group of investigators showed that aging itself is associated with the onset of the elevation of intracellular calcium and reduction of intracellular Mg that is indistinguishable from effects seen in essential hypertension and diabetes mellitus independent of age [28].  These changes may predispose older persons to cardiovascular and metabolic diseases.

Wells et al. [28] identified a previously unknown genetic defect in Mg metabolism in salt-sensitive essential hypertension.  This Mg binding defect results in the inhibition of Mg entry into the cell thereby reducing Mg dependent enzymes from operating efficiently.  The resulting lowering of Mg ATP results in the inability to extrude sodium ions and hypertension develops as a consequence of smooth muscle dysfunction.  The authors also found the Mg binding defect was found in every one of 24 patients with type 2 diabetes suggesting that this defect in Mg transport may be a contributor to NIDDM.  These findings are of possible importance when considered in conjunction with the studies described above [18] [21-24 [26] [27].

Gullestad et al. evaluated 88 healthy Norwegians ages 18 to 66 years using a 30 mmole intravenous Mg load test over 8 hours and measured the 24 hour urinary Mg excretion [29].  They found no correlation between Mg retention and serum Mg or basal urinary Mg.  The Mg retention in these healthy patients was 10.6 to – 4%.  The lowest and highest second standard deviation values were -19.5% and 27.5% respectively.  This result agrees well with the above historical consensus.

Another study by Gullestad et al. [30] on “healthy free-living elderly Norwegians,” mean age 73 ± 6, using the same load test of 30 mmoles of  Mg revealed a retention of 28% compared to 6% in younger controls.  This finding also roughly agrees with the literature and is very interesting when considered in the light of the findings of Barbagallo et al. [27] that elderly people show intracellular calcium and Mg ion concentrations similar to those found in hypertensives and people with diabetes.

A study of Mg deficiency using the “short-term” Mg loading test by Rob et al. [31] revealed that even low dose (0.1 mmole Mg per Kg of body weight) infused over one hour was still able to differentiate Mg adequate patients from renal transplant patients with known Mg deficiency. After treatment with 5 mmoles of Mg per kilogram body weight for four months, a cohort of the latter group reduced their Mg retention from 47% on average to 16%.  The placebo transplant patients continued to retain the infused Mg at 58% of the dose.  The utility of this short-term, low dose Mg retention test can clearly help identify Mg deficiency and help ensure that patients are adequately repleted.

Finally, we could ask which tissue cells are the benefactors of the increased Mg retention in the patients studied.  Bone may be a tissue compartment that may have taken up the infused magnesium since two-thirds of the total body Mg content is contained in skeletal tissue[32].  This is especially likely since it is known that the Mg content of bone falls with age [33] and in the osteoporotic state [34].  If the diet is Mg deficient and the small intestine and kidney can’t effectively increase Mg absorption, bone releases the element into the extra cellular fluid to maintain the serum level [35].

CONCLUSION

These data demonstrate that Mg deficiency may be widespread.  The composition of the infusate used in magnesium load tests appears to have minimal influence on magnesium retention and does not explain the reported magnesium deficiency.  The importance of dietary factors, especially Mg, in the causation of the present epidemic of metabolic syndrome and its associated complications calls for additional efforts to identify and treat patients at risk of magnesium deficiency.

Table 1:  EDTA and cocktail effects on magnesium losses and retention on the day of the infusions (day 3) minus average of days 1 and 2

 

SUBJECT # COCKTAIL COCKTAIL MINUS       EDTA SALINE
1 263 285 345
2 245 156 50
3 203 116 116
4 193 144 198
5 182 210 276
6 133 80 96
7 205 289 268
MEAN ± SEM 203 ± 16 182 ± 31 193 ± 41
% Retention of infused magnesium 70.3 ± 2.3 73.3 ± 4.5 71.9 ± 6.0

 

Values are mean ± SEM.  All infusates contained 686 mg of Mg.

Values for COCKTAIL, COCKTAIL MINUS EDTA and SALINE are urinary magnesium losses (mg) on day 3 minus the average for days 1 and 2.  There were no significant differences among the three different infusates tested.

 

 

 

 

Table 2:  Intravenous magnesium load tests in patients and controls

Reference Country Patients, Mg Retention, % Disease/Condition Controls, Mg Retention, %
Thoren [36]
Caddell et al. [37]
Bohmer & Mathiesen [38]
Ryzen et al. [39]
Fort & Lifshitz [40]
Jeppesen [12]Sjogren et al. [18]
Rasmussen et al. [41]
Martin [42]
Gullestad et al.  [19]
Gullestad et al.  [29]
Gullestad et al. [30]
Ozono et al. [43]
Toral Revuelta et al. [44]
Hebert et al. [45]
Papzachariou et al. [46]
Waters et al. [9] 
Sweden
USA
Sweden
USA
USA
DenmarkSweden
Denmark
UK
Norway
Norway
Norway
Japan
Spain
Canada
UK
USA
>20
51.0
77.0
51.0
58.7
42.062
34.0
62.0
16-38
No patients
28.0
41.9
28.0
70.0
59.8
83.0
G.I. fluid loss
Post partum women
Alcoholics
Alcoholics
IDDM children
MICrohn’s disease
IHD
Elderly
Various diagnoses
No patients
Elderly
Hypertension
Malnourished elderly
Intensive care patients
Pancreatitus
CAD/DM
NC*
NC
22.6
15.0
NC
22.025
4.7
NC
3-4
6.3-10.3
6.0
31.8
Not given
NC
22.0
NC

Citations are in chronological order.

*NC denotes no controls.

ACKNOWLEDGEMENT

 

The authors would like to thank the late Dr. Mildred Seelig for her advice and encouragement during the initial stages of this study.

 

 

 

Reference List

 

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  41. Rasmussen HS, McNair P, Goransson L, Balslov S, Larsen OG, Aurup P (1988) Magnesium deficiency in patients with ischemic heart disease with and without acute myocardial infarction uncovered by an intravenous loading test. Arch Intern Med 148:329-332
  42. Martin BJ (1990) The magnesium load test: experience in elderly subjects. Aging (Milano) 2:291-296
  43. Ozono R, Oshima T, Matsuura H, Higashi Y, Ishida T, Watanabe M, Yoshimura M, Hiraga H, Ono N, Kajiyama G (1995) Systemic magnesium deficiency disclosed by magnesium loading test in patients with essential hypertension. Hypertens Res 18:39-42
  44. Toral R, Jr., Martinez HD, Martinez RM, Llobell SG, Peralba Vano JI, Ribera Casado JM (1996) Intravenous magnesium load test in elderly patients with protein-energy malnutrition. Magnes Res 9:293-298
  45. Hebert P, Mehta N, Wang J, Hindmarsh T, Jones G, Cardinal P (1997) Functional magnesium deficiency in critically ill patients identified using a magnesium-loading test. Crit Care Med 25:749-755
  46. Papazachariou IM, Martinez-Isla A, Efthimiou E, Williamson RC, Girgis SI (2000) Magnesium deficiency in patients with chronic pancreatitis identified by an intravenous loading test. Clin Chim Acta 302:145-154

Address all correspondence to:

Dr. Robert S. Waters, Waters Preventive Medical Center, PO Box 357,Wisconsin Dells, WI 53965, Phone: 608-254-7178, FAX: 608-253-7139, Email: sarah@watershealthcenter.com

 

 

Introduction to Clinical Metal Toxicology

Introduction to Clinical Metal Toxicology

By James Smith DO

INTRODUCTION
The discipline of Clinical Metal Toxicology is evolving and the next 10 years are going to be very exciting. The impetus started with a group of advanced thinking doctors working with forward thinking laboratories and pharmacies, like Medaus Pharmacy in Birmingham, Alabama. Over a quarter century ago these physicians formed the American Board of Chelation Therapy. Today it is called the American Board of Clinical Metal Toxicology. (*Note: this group ABCMT merged with the International College of Integrative Medicine in 2015)

As the story goes, workers were painting warships with leaded paint and became toxic. They began receiving EDTA, a chelating agent, for lead toxicity and it was noted that those who had symptoms of heart disease were showing some improvement. This phenomenon was apparently ignored by conventional doctors but some progressive doctors started using EDTA chelation therapy to treat heart disease. Hence, the smear began! Doctors who did chelation therapy were quacks, charlatans, duping the public. However, not only was a majority of the patients’ cardiac symptoms improving but there were improvements in a myriad of other symptoms and disease processes.

So the line was drawn in the sand. Doctors continued to use chelation therapy to treat their patients, even though they were threatened with loss of their license to practice medicine. They were and still are targeted by medical boards and other establishment organizations.

However, the tide is changing. There presently is a 30 million dollar study, TACT (Trial to Assess Chelation Therapy), to assess the use of EDTA chelation therapy to treat heart disease. We certainly hope that neither politics nor personal predjudices will taint the results of this study.

What are we really looking at when we talk about heart disease or other diseases that respond favorably to chelation therapy? What we are not lookng at is an example of acute intoxication with a toxic metal. What we are observing is some contribution to the disease process by an insidious chronic exposure to toxic metals. The slow, behind the scenes, destruction that toxic metals do to our bodies manifests itself in the form of some disease process. Are all dieases caused by toxic metals? Of course not! But toxic metals contribute, sometimes in a small way and many times in a big way to many pathological processes.

SEMANTICS
The current terminology used is heavy metals or toxic heavy metals. Heavy refers to the atomic weight of the element. For example, molybdenum is a heavy but essential metal, while beryllium is a light but very toxic metal. Additionally, essential metals like calcium can be toxic at supraphysiologic levels and chromium as the Cr+3 ion is an essential trace element important for maintaining correct blood sugar levels, but as the Cr+6 ion is a known human lung carcinogen. Also, arsenic which is considered a toxic metal is really a metalloid, not a metal. At this point I am using toxic metals to describe metals with no known biological function that may disrupt essential physiological processes. Examples of this are cadmium, lead, mercury and arsenic.
TOXIC METALS
Here is a list of toxic metals: Aluminum, Antimony, Arsenic, Barium, Beryllium, Bismuth, Cadmium, Chromium, Cobalt, Gadolinium, Gallium, Lead, Manganese, Mercury, Nickel, Palladium, Platinum, Polonium, Plutonium, Silver, Thallium, Tin, Thorium, Tungsten, Uranium and Vanadium. I recently added Gadolinium because of the suspected problems with MRI dyes.

WHAT ARE METALS?
Chemically, metals including toxic metals are distinguished from non-metals by their capacity to lose electrons, forming positively charged ions, in a chemical process called an oxidation-reduction or redox reaction. When an atom of a metal loses electrons it is being oxidized. The most common example of a redox reaction is the formation of rust. In moist air, iron tends to lose three electrons in a redox reaction with oxygen. When that happens, the iron (Fe) loses electrons (becoming the Fe+3 ion) and oxygen picks them up. Arsenic, the metalloid, possesses this property, also.

WHERE ARE METALS FOUND?
Metals account for a quarter of the Earth’s mass, but a lower percentage of its crust. Sea water contains trace amounts of metals, as do all living organisms and even dust particles in the air. Volcanoes and natural weathering can release metals into the environment, but human activities now play the major role in dispersing metals on the earth’s surface.

Mining and smelting of metal ores can create piles of waste, or tailings, which often still contain relatively high concentrations of metals that can be carried into watersheds or transported by the wind. Metals are also released into the atmosphere from fossil fuel power plants, trash incineration and combustion of leaded gasoline.

The problem with certain toxic metals is that they tend to form very stable and long-lasting complexes with sulfur in biological molecules, which can disrupt their biological function. In some cases this allows these metals to become concentrated at higher levels of the food chain.

WHAT ROLE DO METALS PLAY IN LIVING THINGS?
Many metals play critical roles in maintaining life. Some are important for the structure of biological materials, as calcium is for bone. Other metals stabilize proteins in unique and active conformations or structures. Zinc often performs this function. Magnesium in the form of Mg+2 plays a role in balancing the negatively charged phosphates that serves as the backbone of DNA and RNA.

Metals also serve a chemically important role as essential components of many enzymes. These metalloenzymes are involved in the synthesis, repair and degradation of biological molecules, the release and recognition of certain biological signaling molecules, and the transfer of small molecules and electrons in crucial processes such as photosynthesis and respiration. For example, iron-containing hemoglobin transports oxygen in blood.

WHAT MAKES METALS TOXIC?
The toxic effects of most metals can be traced to their ability to disrupt the function of essential biological molecules, such as proteins, enzymes and DNA. Biological molecules have specific structures and certain components that are essential for their roles. If this structure is altered or a specific part of the protein becomes damaged, then it may no longer be able to carry out its necessary role. If a metal ion binds to the amino acids of a protein, the resulting metal-protein complex may lack the protein’s original biological activity. Certain toxic metals have a high affinity for sulfur and will bind tightly to the essential cysteine, inhibiting the enzyme from functioning. One toxic metal may also substitute for another similar essential metal. For example, the toxic metals, mercury and cadmium, can substitute for the essential metals, zinc and selenium. Similarly, lead can substitute for calcium and iron.

In some cases the disruption of a few biological molecules has an amplified effect. One example is the transcription factor proteins that, in response to a signal, bind to DNA and initiate the synthesis of new proteins required for development, normal cellular metabolism or response to some stress. Another example is enzymes, the biological catalysts that are needed in only small amounts but which play essential roles in all biological processes. A third example is proteins that are involved in the repair of damage to biological molecules. While most damaged proteins are simply replaced, DNA must be repaired if the information in an organism’s genome is to remain intact. Disruption of DNA repair leads to propagation of errors in an organism’s blueprint.
Living organisms have also developed mechanisms for dealing with certain toxic metals and toxic levels of essential metals.

METALLOTHIONEINS (MTS)

These are low molecular cysteine rich proteins. One of the primary roles of MTs is toxic metal detoxification. Also, MTs are involved in the homeostasis of copper and especially zinc ions. MTs are significant antioxidant and antiapoptotic proteins. They are also involved in the control of the redox status of cells and in energy metabolism. As a consequence of their high cysteine content, they serve as a toxic metal detoxification system for mercury, cadmium and silver. The affinity of the metal ions for the binding sites is: mercuryII> silverI> copperI> cadmiumII>zincII. The goal of the MTs is to do their work in the cytosol and keep the toxic metals away from the mitochondria and nucleus of the cell. With toxic exposure there is an up regulation in production of the MTs.

RESEARCH
There has been a lot of research done on the toxic metals, mostly in animals. It shows that they are endocrine toxic, developmental and reproductive toxic, immunotoxic, cardiovascular toxic, neurotoxic, genotoxic, carcinogenic, hepatotoxic and nephrotoxic. Also, we are seeing more papers in the peer reviewed journals based on live patients.

A study on Marked Elevation of Myocardial Trace Elements (TE) in Idiopathic Dilated Cardiomyopathy Compared with Secondary Cardiac Dysfunction in the journal of the American College of Cardiology in 1999 found that a large, significant increase of myocardial (endomyocardial biopsy) TE several times normal (mercury at 22,900x, antimony at 12,800x, arsenic at 250x) was present in IDCM but not in secondary cardiac dysfunction and the increased concentration of TE in patients with IDCM may adversely affect mitochondrial activity and myocardial metabolism and worsen cellular function.

MERCURY
Some major sources of contamination are fossil fuel burning factories, breast feeding and dental amalgams.

Some of the general symptoms of toxicity are chronic fatigue, not improved with rest, depression, increased irritability, nervous excitability, moodiness, inability to concen-trate, loss of memory, insomnia or drowsiness, vertigo, tinnitus, headache, twitching, lack of coordination, gait disturbances, muscle pain and body aches, mild nasal congestion, stuffy nose, hair loss, swollen lymph nodes around the TMJ area with tenderness, dark pigmentation of the gums, tremors, hyporeflexia of the lower extremities, bruxism, and metallic taste in the mouth.

A study on Methylmercury in the New England Journal of Medicine in 2003 found that the fetal brain is more susceptible than the adult brain to mercury-induced damage and mecury inhibits the division and migration of neuronal cells and disrupts the cytoarchitecture of the developing brain.

A study on Methylmercury & Inorganic Mercury in Pregnant Women & in Cord Blood: From Fish in Environmental Health Perspectives in 2003 found that both hair total mercury and cord blood methylmercury increased with increasing consumption of seafood and that inorganic mercury in cord blood increased significantly with increasing number of maternal dental amalgam fillings.

A study on Mercury’s Link to Heart Disease Begins in Blood Vessel Walls in the International Journal of Toxicology in 2007 found that mercury’s link to heart disease can be traced to activation of an enzyme, phospholipase D (PLD), which triggers a process leading to plaque buildup in blood vessel walls. Types of mercury compounds studied were methylmercury chloride, (environmental), thimerosal (pharmaceutical) and mercuric chloride (inorganic). Chelation & antioxidants helped and this is a model for other toxic metals also.

A study on Apolipoprotein-E Genotyping as a Potential Biomarker for Mercury Neurotoxicity in the Journal of Alzheimers Disease in 2003 found that apolipoprotein-E genotyping has been investigated as an indicator of susceptibility to heavy metal (i.e., lead) neurotoxicity, a statistically relevant shift toward the at-risk apo-E4 groups was found in the patients (p<0.001). The patients possessed a mean of 13.7 dental amalgam fillings and 31.5 amalgam surfaces and confirmation of an elevated body burden of mercury was made by measuring urinary mercury, after provocation with DMPS and this was measured in 150 patients.

A study on Mercury from Fish, Lipid Peroxidation & the Risk of Myocardial Infarction & Cardiovascular Disease & Death in the journal of Circulation in 1995 found that a high intake of mercury from non-fatty freshwater fish and the consequent accumulation of mercury in the body are associated with an excess risk of acute MI as well as death from coronary heart disease, CVD, and any cause in Eastern Finnish men and this in-creased risk may be due to the promotion of lipid peroxidation by mercury.

A study on Mercury, Fish Oils & the Risk of Myocardial Infarction in the International Journal of Toxicology in 2003 found that the toenail mercury level was directly associated with the risk of MI, the adipose-tissue DHA level was inversely associated with the risk and high mercury content may diminish the cardio-protective effect of fish intake.

A study on Reduced Levels of Mercury in First Baby Haircuts of Autistic Children in the International Journal of Toxicology in 2003 found that, the reduced levels of mercury in the first baby haircut of autistic infants raises clear questions about the detoxification capacity of this subset of infants and despite hair levels suggesting low exposure, these infants had measured exposures at least equal to a control population, suggesting that control infants were able to eliminate mercury more effectively.

LEAD
Some major sources are leaded gasoline, lead-containing paint, cigarettes, water (lead pipes and lead solder), food and air. The half-life of lead in the body is 25 days in blood, 40 days in soft tissue and 20+ years in bone.
(*missing graphic)
Adapted from ASTDR Toxicology Profile for Lead 1989
Toxicology of Metals, 1996, Louis W. Chang, pg 517

A study on Blood Lead and Hypertension in Peri-menopausal & Post-menopausal Women in the Journal of American Medical Association in 2003 found that at levels well below the current US occupational exposure limit guidelines (40 μg/dL), blood lead level is positively associated with both systolic and diastolic blood pressure and risks of both systolic and diastolic hypertension among women aged 40 to 59 years, the relationship between blood lead level and systolic and diastolic hypertension is most pronounced in postmenopausal women and these results provide support for continued efforts to reduce lead levels in the general population, especially women.

A study on Blood Lead Below 0.48 µmol/L (10 µg/dl) and Mortality Among US Adults in the journal of Circulation in 2006 found that the association between blood lead levels and increased all-cause and cardiovascular mortality was observed at substantially lower blood lead levels than previously reported and despite the marked decrease in blood lead levels over the past 3 decades, environmental lead exposures remain a significant determinant of cardiovascular mortality in the general population, constituting a major public health problem.

A study on Intellectual Impairment in Children with Blood Lead Concentrations below 10 µg/dl in the New England Journal of Medicine in 2003 found that blood lead concentrations, even those below 10 µg per deciliter, are inversely associated with children’s IQ scores at three and five years of age, and associated declines in IQ are greater at these concentrations than at higher concentrations and these findings suggest that more U.S. children may be adversely affected by environmental lead more than previously estimated.

A study on Low Level Environmental Lead Exposure and Children’s Intellectual Function: an International Pooled Analysis in Environmental Health perspectives in 2005 found that for a given increase in blood lead, the lead-associated intellectual decrement for children with a maximal blood lead level < 7.5 μg/dL was significantly greater than that observed for those with a maximal blood lead level ≥ 7.5 μg/dL (p = 0.015) and we conclude that environmental lead exposure in children who have maximal blood lead levels < 7.5 μg/dL is associated with intellectual deficits.

ARSENIC
The use of arsenic is dropping off because of its toxicity. Some major sources are 90% used as wood preservative (although this too is being phased out), silicon based computer chips, feed additive (poultry and swine), cotton fields, chemotherapeutic and some in food and water.

Some of the general symptoms of toxicity are headache, drowsiness, fatigue, chronic fatigue syndrome, confusion, brittle nails, follicular dermatitis, hoarse voice, pigmented spots on trunk, Raynaud’s syndrome (poor circulation to extremities), weakness and muscular atrophy and palmar and plantar keratoses, atypical (pre-cancerous) keratoses on hands, feet, and trunk.

One route of elimination of inorganic arsenic which is more toxic than the organic form is As5+ (Arsenate) to As3+ (Arsenite) to Methylarsenite (in liver) to Dimethylarsenite which is readily eliminated – urine.

A study on Folic Acid Supplementation Lowers Blood Arsenic in the American Journal of Clinical Nutrition in 2007 found that folic acid supplementation to participants with low plasma concentrations of folate lowered blood arsenic concentrations, primarily by decreasing blood monomethylarsonic (MMAs) and increasing urinary dimethylarsinic (DMAs) acids and therapeutic strategies to facilitate arsenic methylation, particularly in populations with folate deficiency or hyperhomocysteinemia or both, may lower blood arsenic concentrations and thereby contribute to the prevention of arsenic-induced illnesses.

A conclusion in the CA Cancer Journal for Clinicians in 2001 stated that there is strong epidemiological evidence that arsenic is a human carcinogen. Inhaling arsenic increases the risk of lung cancer and ingesting arsenic increases the risk of skin, urinary tract, and lung cancer. Based on this evidence, expert agencies have classified arsenic as a human carcinogen. Because of the cancer risk and other health hazards associated with arsenic, exposures to arsenic should be minimized.

CADMIUM
It is toxic to every body system and accumulates in body tissue. There is concern about the increase in environmental cadmium that has occurred as a result of its increasing industrial use. Inhaled is better absorbed than ingested. Elimination rate is generally very slow and the toxicity is significantly influenced by dietary intake of other elements such as zinc, copper, and selenium.

Some of the general symptoms of toxicity are fatigue, chronic fatigue syndrome, hypertension (possibly related to increased concentration of cadmium in renal parenchyma), iron deficiency anemia, osteomalacia in parous women over 40 years of age with dietary deficiencies, anosmia (loss of sense of smell), yellowing of teeth, reduced birth weight in newborns, renal colic (with passage of calculi), nephrocalcinosis, hypercalcuria, emphysema and liver damage.

Some of the major sources are drinking water, soft water, causing uptake of cadmium from galvanized pipes, soft drinks from vending machines with cadmium piping, refined wheat flour (increased cadmium:zinc ratio), batteries (Ni-Cd), evaporated milk, many processed foods, oysters, kidney, liver, rice (irrigated by Cd contaminated water), cigarettes and tobacco, super-phosphate fertilizers, cadmium alloys (e.g. dental prosthetics), ceramics, paint pigments (yellow tint) and electroplating.

A study by the National Swedish Institute of Environmental Medicine and Department of Environmental Hygiene concluded that smokers have higher concentration of cadmium in their blood than non-smokers.

METAL BINDING AGENTS
They have been developed over the last 50 years. An ideal MBA would mobilize the toxic metal and increase its excretion through the kidneys as a water soluble complex. There have been tens of thousands of metal binders created but only a dozen in use. They are underutilized.

The major natural pathway for excretion of toxic metals is via the liver, gall bladder and into the stool. With an acute toxic overload you can detect metals in the urine.

This is a schematic diagram of how EDTA which has 6 potential negative sites engulfs a metal ion and carries it out of the body via the kidneys.

EDTA

In disodium EDTA the sodium was added to make the molecule more water soluble. It is used for treatment of ventricular arrhythmias and hypercalcemia.

Calcium disodium EDTA is used primarily for lead poisoning and does not interfere with serum ionized Ca. It is safe to use in little children. However, all available product is contaminated with aluminum.

EDTA is used intravenously and will bind chromium, iron3+, mercury, copper, lead, nickel, zinc, cadmium, cobalt, aluminum, arsenic, iron2+, calcium, magnesium and molybdenum.

DMSA

It is used orally and will bind with mercury, methylmercury, copper, lead, nickel, zinc, cadmium, silver, and arsenic. It is 50 times less toxic than BAL and 5 times less toxic than EDTA. It does not affect essential minerals except zinc but less than EDTA. It works extracellular but does cross the blood brain barrier.

DMPS

It is used orally and intravenously and will bind with mercury, methylmercury, copper, lead, nickel, zinc, cadmium, silver, and arsenic. It is less toxic than BAL. It does not affect essential minerals except zinc but less than EDTA. . It works extracellular but does not cross the blood brain barrier. It is excreted by the kidneys.

GLUTATHIONE (l-glutamylcysteinylglycine)

Glutathione is found almost exclusively in its reduced form, since the enzyme which reverts it from its oxidized form (GSSG), glutathione reductase, is constitutively active and inducible upon oxidative stress.

Each molecule of a toxic metal takes out 2 molecules of glutathione.

Functions
• Intracellular antioxidant.
• Essential donor of sulfhydryl groups necessary for the detoxification of the liver
• Enables conversion of Phase I Detox products to water-soluble forms
• Facilitates cell carbohydrate metabolism, calcium metabolism, blood platelet and membrane functions.
• Involved in amino acid transport across cell
• Part of the peptidoleukotrienes.
• Cofactor for enzymatic reactions
• Aids rearrangement of protein disulfide bonds
• DNA synthesis and repair
• Prostaglandin synthesis
• Metabolism of toxins & carcinogens
• Immune system enhancement
• Essential for thyroid hormone synthesis of T4 to T3
• Essential for hair growth

PROVOCATIVE URINE
Also called a urine challege, it consists of giving the patient a dose of a metal binding agent (chelating agent) and collecting a urine sample for a set period of time. The urine is then sent to the lab to determine the metals that have been pulled out of the body by the MBA.

This has been recognized as a valid test by the CDC and independent researchers to evaluate the patient’s metal load when one is not concerned about acute toxicity. When used to evaluate smokers we always find high levels of lead and cadmium.

IN CONCLUSION
The bottom line is that we have to get more patients checked for metal toxicity. As discussed we are concerned about chronic toxicity. The science available does correlate with the clinical findings in the office once you start paying attention to metal toxicity. The process of challenging for metals and subsequently treating the patient to remove the metals is a very safe procedure when done properly. Removing this source of oxidative stress and inflammation is certainly a good beginning to ridding your patients of degenerative disease processes. I would encourage any physician interested in learning more about diagnosing and treating metal toxicity to contact the American Board of Clinical Metal Toxicology (www.abcmt.org).

PROTOCOLS

TOXIC METAL CHALLENGE
• No fish or dairy for 3 days before challenge
• No minerals or SH containing supplements for 24 hours before challenge
• Serum creatinine must be normal
• Reinforce nutritional status
• Collect a pre-challenge urine sample
• DMSA 500 mgs. orally
• 100 cc NS, extract air, add DMPS 125 mgs. and run in over 20-30 minutes
• 100 cc NS, add Ca Disodium EDTA 3000 mgs. (1 hr.)
• Empty bladder prior to IV then collect 6 hour urine sample and ship to lab

DMSA – DETOXIFICATION – 14 DAY CYCLE
• No minerals 24 hrs prior to or during taking of DMSA
• Avoid fish for 3 days
• Oral DMSA at 10 mg/kg tid for 3 days (500 mgs. Max)
• Off for 11 days
• Average is 5-10 cycles
• Take minerals and SH-containing supplements 24 hrs after last dose
• Perform provocative test about every 5th cycle

DMPS – DETOXIFICATION – 14 DAY CYCLE
• Stop mineral and SH-containing supplements for 24 hours prior to dosing
• Avoid fish for 3 days
• Oral DMPS at 100-200 mgs tid or 10 mg/kg in 3 divided doses
• Take for 3 days followed by 11 days off
• Take minerals and SH-containing supplements 24 hrs after last dose
• Average is 5-10 cycles
• Perform provocative test about every 5th cycle

EDTA (DISODIUM) – TYPICAL IV BAG
• 500 cc of sterile water
• Use 250 cc bag if fluid is a problem
• Vitamin C 500 mg/cc, to adjust osmolarity above 290, usually 14 cc – 20 cc (500 cc bag)
• Sodium bicarbonate at ½ the EDTA dose in milliliters
• MgSO4 – 4 cc or MgCl2 – 10 cc
• Lidocaine 2% – 2 cc
• Heparin 5000 u/cc – 0.5 cc
• Calculated dose of EDTA based on height,, weight and serum creatinine
• B-Complex – 1cc
• B1-100 mgs, B2-2 mgs, B3-50 mgs, B5-2 mgs, B6-50 mgs, B12-1 mg, FA-1 mg

GLUTATHIONE INTRAVENOUS
IV Push
• Do a 5 cc IV flush of NS or Sterile water
• Administer 100 – 1000 mgs slow IV push at end of Challenge IV, EDTA IV or V/M IV to aid in detoxification
• Flush line with another 3-5 cc of NS or Sterile water
IV Bag
• Use a 100 cc bag of NS
• Add 1000 – 2000 mgs. Of GSH
• Run in over 30 – 45 minutes

REFERENCES
Environmental Health Perspectives – www.ephonline.org
Dartmouth Toxic Metals Research Program – www.dartmouth.edu /~toxmetal/
Agency for Toxic Substances & Disease Registry – www.astdr.cdc.gov/toxpro2.html
Center for Air Toxic Metals – http://www.undeerc.org/catm/health.html
American Board of Clinical Metal Toxicology – http://www.abcmt.org
Toxicology of Metals, 1996, Louis W. Chang
Comprehensive Coordination Chemistry II, Volume 8, pp 213–228

BIOGRAPHICAL INFORMATION
Dr. Jim Smith is a fully licensed Osteopathic Physician with 20 years experience in Family and Emergency Medicine. He has been doing Integrative – Advanced Medicine for 15 years. He is in a full-time practice in Advanced Medicine in the Cincinnati, Ohio area. He is certified in Family Medicine and Clinical Metal Toxicology (Chelation Therapy). He serves on the Board of the International College of Integrative Medicine (www.icimed.com) and the American Board of Clinical Metal Toxicology (www.abcmt.org). He is a member of the Advanced Medical Education and Services Physician Association (www.amespa.org) and the American Osteopathic Association (www.osteopathic.org). He is 1 of 45 physicians in the world who has completed the extensive AMESPA physician training course and has earned the right to be called a Center for Advanced Medicine.

Lead In The Water – Is It Time To Freak Out?

John Parks Trowbridge M. D., FACAM

The simple answer is … it’s not so simple. But you must pay attention to what is happening to you and your family to be able to respond accordingly.

Over 27,000 innocent children in Flint, Michigan, have been exposed to startlingly high levels of lead in their city water supply – sometimes 13,000 times the concentration found in nearby localities – for many months, without any warning, even without early official acknowledgment when the problem was identified. Now city dwellers are left with corrosive toxins leaching from their pipes for who knows how long.

So how can you really know “what is happening”? That is the hard part. So let’s make it easier for you to see it right now.

Recent reports suggest that the major “toxic exposure” is to lead. Quite honestly, it is impossible for just lead to be the only poison to which you’re being exposed during this event. Over time, scientists will determine and share their additional discoveries with the public, so that even better treatments can be offered.

Is it true that younger children can suffer more serious damage from lead exposure? The answer “yes” is simple for you to see: brain and nerves and other organs are rapidly developing … and lead strikes right in the middle of these. The results of such poisoning can be horrific.

Studies reported since the early 1980s have documented that higher lead levels in the body “led directly to” falling IQ. Kids sometimes “act dumb” when they’re fooling around – but the tragedy of becoming a permanently “dumb adult” due to preventable brain damage is a life-destroying lifelong handicap.

How will you recognize more serious lead exposure problems? How about decreased bone and muscle growth and poor muscle coordination? Speech and language problems show up along with developmental delay, even seizures and damage to the nervous system and hearing, even to kidneys. Lower but still toxic levels can be seen as irritability or behavioral issues, difficulty concentrating, headaches, loss of appetite with sluggishness or fatigue; belly pains can show with nausea, vomiting, and constipation. Skin color can be pale due to anemia. Some complain of muscle and joint weakness or pain, also a metallic taste.

Adults can show similar system problems, additionally developing as high blood pressure, heart disease, leg circulation diseases and gangrene, declining mental function, memory loss, headaches, mood disorders, changes in sperm counts and even miscarriage or premature birth. Other heavy metals or chemical toxins (even from yeast/mold) can worsen symptoms such as this or create even other discomforting issues.

Sadly, there’s no treatment available for this poisoning. Wait! – that’s not true! But that is exactly what many worried patients (and parents) will hear from their local doctors in Michigan or around the country – “everyone knows that lead poisoning is irreversible.” Commonly used blood testing is almost useless and rarely confirms toxic metal levels. Accurate diagnosis and precise treatment of heavy metal poisoning – such as with lead, mercury, arsenic, nickel, cadmium, even aluminum and others – is a specialty in medical practice that has evolved over the past 60 years.

What are the TWO key factors that are critical to remove lead that is starting to damage body tissues? First, you need management by a physician who understands and offers a treatment called “chelation” (key-LAY’-shun). FDA-approved medications are available to remove toxic metals – and that is the only effective treatment, nothing else works, not drugs, not surgery, not anything else.

Second, you need chelation treatment that is started early enough and continued long enough. During this treatment program, your specialist will include nutritional supplements to replace “usual” minerals (such as magnesium, zinc, others) that are removed during the treatment for toxic metals, along with vitamins that help to reverse changes due to the poisoning.

The biggest problem that many patients and parents will face is … that doctors and others who have no experience with, or any understanding of, lead poisoning and chelation therapy can discourage you from seeking such treatments. Delay in starting treatment of sudden exposures can result in permanent limitations of brain functions – thinking, intelligence, learning, memory, reasoning, then school performance and later career choices – for a child who depends on his parents to rely on physicians who can find out quickly what is going on and can fix it right.

How successful is chelation therapy at reducing lead deposited in children? Medical studies for years have shown overall excellent results in children when proper treatment is continued as long as each particular patient needs. Each year, over 300.000 young children are found to have unsafe levels of lead in their blood; more definitive tests – urine “challenge” testing, hair analysis – would reveal even more. Adults have already had dozens more years to accumulate lead and other toxic heavy metals from so-called “acceptable” levels in the food, water, and air. Their program is longer because their body burden is much more than just from the recent exposure to poisoned water.

How critical is it for you to avoid further exposure right now? Absolutely required! So you must heed precautions offered by local public health officials. You might need to follow these preventive steps for quite a long time. Tainted water can seep into the underground water table, leading to long term unexpected exposures such as well water, foods from gardens or even farms, public water such as swimming pools or local ponds, rivers, lakes, even city water supplies. What is worrisome is that poisons spread through the environment are much more difficult to remove and might linger for years, causing continuing health challenges long after any “cleanup” has been declared to be completed. The dangers are very real even though invisible.

Did you know that you can “see” and even “smell” lead-laden water, so you can easily avoid drinking it or using for cooking or bathing? That is a myth, pure bunk, a total lie. The only way to protect your children and yourself from continuing poisoning in Flint is to pay attention to recent local water testing that documents the level of toxic heavy metals found over time. Only in this way can you take needed steps to insure pure water and foods for your family – even if you need to make those changes for many months after the cleanup has been reported as concluded.

Is someone to blame for this serious event? Of course. Investigators will find someone who “did something wrong,” that’s obvious. But your usual environment has already been a dangerous place for the last 60 years or more. Lead paints so common in the past (toddlers chewing on window sills or toys), lead gasoline (still used for small airplanes), lead pipes and bootleg stills (lead solder) are easy examples, often explaining gradual toxic accumulations seen now in adults. The Flint water poisoning is a more acute event that suddenly changes everything for a large number of unsuspecting people – infants, children, and adults of all ages – adding further to their underlying body burden of lead and other toxic metals already accumulated over their lifetime.

Is there a bright spot in this disastrous event? Only this: many thousands more people will learn now of the tremendous healing powers of chelation therapy. A few hundred physicians around the country have been trained to deliver chelation therapy, and various approved drugs are available. Beyond rescuing exposed children from a lifetime of lower potential and performance, the reduction of toxic heavy metals by chelation has been documented to improve a wide variety of conditions in virtually every organ. Reducing right now the lead levels in exposed children is essential to minimize or delay later crises as adults suffering heart attacks, high blood pressure, leg artery diseases and gangrene, loss of vision, and much, much more.

Who will really care about your family and your situation in the future? The “news cycle” will soon move on to other headlines and you will be left stranded with the tattered remains of your life. Take advantage now of this opportunity to find a specialist who could help you with your poisoning problems. To consult with a specialist physician who has training in chelation therapy, contact the International College of Integrative Medicine (www.chelation.me) or the American College for Advancement in Medicine (www.acam.org). Be diligent in your search and review the doctor’s credentials conscientiously. Remember: your toxic metal problem (from whatever source) is a serious health challenge and needs treating now … it’s urgent to get the lead out!

ICIM member John Parks Trowbridge M. D., FACAM, has been recognized as a specialist in chelation therapy since1985. Recognized as an expert in various fields of integrative/”alternative” medicine, he has served as a leader of several professional organizations, has written books and published CDs and DVDs, and has lectured across the country and around the world.

CONTACT: 281-540-2329, telefacsimile 281-540-4329
speciallch@earthlink.net, info@healthCHOICESnow.com