Administrator, Author at Intravenous Disodium Edetate ("chelation")

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?

February 20, 2016February 20, 2016 by Administrator

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

DenmarkSweden

Denmark

Norway

Japan

Spain

Canada

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

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.

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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
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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

February 20, 2016February 21, 2016 by Administrator

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?

February 2, 2016February 23, 2016 by Administrator

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

An Open Letter to Cardiologists

July 23, 2015 by Administrator

Dear Cardiologist,

My name is Dr. Bruce Dooley and have I practiced in Fort Lauderdale and Naples for twenty years. Having recently arrived in Palm Beach County, I am writing to all the local Cardiologists to both personally introduce myself as well as seeking your cooperation and participation in an outcomes study involving EDTA Chelation Therapy. I will describe this in more detail in a minute.

You may be aware of the recent significant clinical results of the 7-year Trial to Assess Chelation Therapy (TACT). This randomized, double-blinded, placebo-controlled study was funded by the NIH and headed up by Dr. Tony Lamas (Chief of Cardiology, Miami Mt. Sinai Hospital). At the November 2012 Annual meeting of the AHA, Dr. Lamas announced that the study proved that EDTA intravenous therapy was both clinically effective and safe. Regrettably, the response from the Cardiologists on the panel was that “more studies were needed“.

Having personally supervised the administration of over 10,000 EDTA infusions, I and other physicians knowledgeable on this therapy were not surprised by the positive results of the TACT study: Improvements in circulation are the norm and were first discovered in the early 1950’s followed by much interest and investigation of this intravenous therapy . But when EDTA (ethylene diamine tetra acetate, (commonly used to chelate lead and other metals) lost its patent and became generic in the 1960’s, Abbott Labs dropped their research for its approval as a cardiac drug. It is also important to note that it was during this period that Dr. Michael DeBakey performed the first CABG in Houston. Thus, for the past 50 years, physicians like me have performed this therapy, formed medical associations to develop safe protocols, and train other physicians. Many office-based outcome studies were published and the vast majority showed significant improvements in circulation. But a properly constructed study was needed to convince other physicians of the effectiveness and safety of EDTA chelation.

So here our present dilemma and my reason for requesting your help: Getting the NIH to fund this $35 million TACT study in 2003 was difficult enough. We seriously doubt that further monies will be forthcoming. There was also the problem of patient recruitment (ask a person to sit in a recliner chair for 40 treatments for three hours each with a 50% chance it is a placebo). The question then arose as to how to gather more data now that EDTA chelation therapy has been proven clinically effective and safe. One consideration was to seek other physicians help to enrol their eligible patients in an outcomes study. Our belief is that if enough evidential outcomes are positive as reviewed and submitted by respected Cardiologists, then this therapy may gain acceptance as a recommended treatment.

So we see this happening as such:

1. Participating cardiologists refer a patient for a series of twenty EDTA chelation infusions with the cost of the program being born by the patient, who is given full informed consent.

The participating referring cardiologist completes both a pre and post chelation program evaluation for which he/ she will be directly reimbursed $500 as remuneration for their time spent on the evaluations (total of 20-30 minutes). This will be paid to the physician at the onset of the twenty treatment program by their patient.
On a national level, this program would generate a significant number of reports from Cardiologists which would eventually be collated into a report and submitted to the American Heart Association for their consideration.
I am seeking your help by becoming a participating physician in this important project. To better get acquainted with each other, and to further explain the therapy, please allow me the opportunity to meet with you outside of your busy office practice. It would be my pleasure to show you our beautiful center and answer any questions you might have over dinner if you like.

To help facilitate this, I would request that you please return the enclosed, stamped response card indicating your decision to either accept or decline participation. If you would like to participate, I will have my staff do a follow- up call to your office to schedule an afternoon visit/dinner.

Thank you very much for your time and attention and I look forward very much
to hearing back from you.

Kind regards,
Dr. Bruce Dooley

A Comprehensive Integrative Approach to Diabetes

July 23, 2015July 23, 2015 by Administrator

By L. Terry Chappell, T. Rae Neal, Natallie Paphanchith

Incidence and Cost

Diabetes is a growing epidemic in the United States. According to the National Diabetes Statistics report for 2014, 21 million people in the United States have been diagnosed with type 1 or type 2 diabetes. It is estimated an additional 8.1 million people are undiagnosed. In addition to diabetes, 86 million Americans were diagnosed with the precursor, pre-diabetes in 2012. Treatment and management of this disease is costly. The estimated annual cost of diabetes per year in the US is 245 billion dollars.

More alarming than diagnosis and cost is the impact diabetes has on our overall health and wellbeing. Diabetes was listed as the 7^th leading cause of death in the United States in 2010. When diabetes is controlled we reduce the risk of co-existing diseases. Unfortunately, many patients remain with an elevated hemoglobin A1C. Uncontrolled diabetes leads to multiple micro and macro vascular complications. Co-morbidities secondary to diabetes include: hypertension, hyperlipidemia, coronary artery disease, cerebral vascular accidents, chronic kidney disease, amputation, retinopathy, and neuropathy (1).

Conventional Approach to the Treatment of Diabetes

Type 2 diabetes mellitus (T2DM) is clearly linked to obesity. As obesity rates climb, so does the diagnosis. 80-90 percent of patients diagnosed with type 2 diabetes are classified as obese. The International Diabetes Foundation was quoted, “Diabetes and obesity are the biggest public health challenges of the 21^st century”. The link here is clear; obesity drives insulin resistance and an inflammatory response. Prolonged insulin resistance puts an extreme amount of stress on the pancreas. When resistance is accompanied by dysfunction of the pancreatic islet b cells that is what ultimately leads to the disease (2).

A dietary goal should be to minimize refined sugars and starches. Modern carbohydrate staples, like potatoes, breads, and cereals, have a high glycemic index (GI) and a very strong link to chronic disease (3). Foods low on the GI scale like sweet potatoes, winter squash, and beans help to stabilize blood glucose levels. This can be achieved with whole structured foods and lower GI. Clinical trials support low GI diets with greater fat content as more effective than low fat diets at preventing complications associated with cardiovascular disease. Often a low fat diet contains the highest GI content, which leads to increased insulin resistance. Low GI diets improved whole body insulin sensitivity throughout the trials with no increase in LDL cholesterol (3). Whole rice and seeds decrease circulating levels of glucose, insulin, LDL cholesterol, and fructosamine, while refined sugar and high fructose corn syrup lead to increased risk for T2DM. Large amounts of fructose result in insulin resistance and could accelerate the development of T2DM and associated complications. Avoiding processed foods is an important step in preventing and managing diabetes (4).

Many treatment options are available to treat diabetes. Since discussing obesity in the previous paragraph, lifestyle modifications are the initial target. Nutritional planning, weight loss and diabetic education are a top priority. However, despite efforts of diet and exercise many patients will require additional therapies. There are multiple oral medications. Metformin is the initial medication of choice if liver and kidney function remain stable. However if the hemoglobin A1C remains elevated after 3 months of therapy an additional agent may be selected. Treatment of diabetes has greatly changed in the last 10 years. Use of Sulfonylureas, Meglitinides and Alpha-glucosidase inhibitors are less common as innovative medications are integrating to the market.

Emerging drug classifications include Thiazolidinediones, DPP-IV inhibitors, GLP agonists, and SGLT2 inhibitors. If insulin resistance remains high and oral medications and injectable non-insulin medications are not effective in maintaining glycemic control, insulin may be added. Likewise, if chronic medical conditions arise and prevent the use of certain medications, a basal bolus regimen of insulin may be more appropriate.

Goals of Treatment

As previously mentioned, treatment goals are targeted by the hemoglobin A1C. The A1C is a 3 month average of the patients’ blood sugar. An A1C less than 5.7 percent is normal, prediabetic range is 5.7-6.4 percent and diabetes is diagnosed if the A1C is greater than 6.5 percent. For patients diagnosed with diabetes The American Diabetes Association recommends an A1C goal less than 7 percent. However, many randomized trails that examined the effects of glycemic control excluded the frail elderly (5).

Newer data points to higher health threats in the elderly population with tight glycemic control. The most common risk is severe hypoglycemia. Hypoglycemia leads to increased falls, injury, trauma, and hospitalizations (6). Also, elderly patients are more likely to experience adverse effects from their medications. The American Geriatric Society recommends the targeted A1C to be 8% in the elderly (7). However, the A1C target is controversial among various organizations. Ultimately, goals should have an individualist approach and target.

Complementary Treatment Options and Lifestyle Measures

Complementary, alternative, integrative, or comprehensive, whatever term you choose, these additional approaches to medicine offer many options for the prevention and treatment of T2DM. The California Institute of Integral Studies and Integrative Medicine presented a paradigm shift in our health care system at the International Congress for Clinicians in Complementary and Integrative Medicine in 2013 (8). Collaborative practice and interaction between disciplines will provide valuable insight toward a new health care model. It is estimated that as much as 40% of adults use complementary and alternative medicine (CAM) with up to 34% of those patients having a chronic disease. These figures are deceptive when disclosure of CAM use is often withheld due to conflict with other providers (9).

Personal responsibility is essential for prevention and management of diabetes. Awareness of recommended caloric intake and ideal body weight prevent the buildup of excess body fat, which can lead to cellular insulin resistance. Maintaining ideal body weight and modifying the diet to include important nutrients, limit less beneficial ingredients, and eliminate harmful options will lead to improved glycemic control(4). Organic pollutants also accumulate in adipose tissue and carry destructive consequences. Sorbitol accumulation caused by environmental exposure leads to cell death and contributes to diabetic complications (4). Weight loss and detoxification will improve insulin sensitivity and glucose tolerance. Losing as little as 5% of body fat leads to marked improvement in glycemic control and reduces the incidence of T2DM by up to 50% (10).

Gaby also identified a gluten free diet as delaying or preventing the development ofT2DM due to the preservation of beta cells. Vegan diets improve glycemic control. Coffee is associated with a decrease risk of developing T2DM. Oolong tea is associated with a mean decrease in plasma glucose concentrations. This could be due to reducing iron absorption, which might improve glycemic control. Modest increases in body iron stores have an adverse effect on glucose metabolism. Iron depletion enhances glucose utilization. Phlebotomy treatments have effectively reduced iron concentration to vegetarian levels and caused a 40% increase in insulin sensitivity (4). Deferoxamine, an iron-chelating agent, was used in poorly controlled diabetic patients with elevated ferritin levels successfully to improve blood glucose and HbA1c levels (4).

Increased dietary fiber from legumes, carrots, artichokes, peaches, strawberries, and grapefruit can improve glycemic control. Obtaining fiber from food is preferred. If supplementation is necessary, unprocessed wheat bran or apple fiber are recommended. Legumes have an ability to flatten blood sugar response for over four hours, when eaten at breakfast. The blood sugar remained consistent four hours after ingestion (4).

The temperature and manner in which food is cooked plays a role in the development of diabetes. The advanced glycation end products (AGE) remain in food after the cooking process. These products cause modifications in protein structure, which promote inflammation (4). Less AGE formation results from cooking techniques using water at low temperatures for a longer period of time. An emphasis on boiling, poaching, and stewing over frying, broiling, and roasting can decrease AGE by up to 50%. AGE products play a role in the pathogenesis of insulin resistance and diabetic complications (4).

Effect of acidic environment on the advanced glycation end product (AGE) content of beef. Beef (25 g) was roasted for 15 minutes at 150°C with or without premarinating in 10 mL vinegar (A) or lemon juice (B) for 1 hour. Samples were homogenized and AGE (N^ε-carboxy-methyl-lysine) content was assessed by enzyme-linked immunosorbent assay as described in the Methods section. Data are shown as % change from raw state. White bars represent raw state, hatched bars roasted without marinating and black bars marinated samples. *Significant changes compared to the raw state (P<0.05). ^#Significant changes compared to cooked without marinating samples. 1=raw beef. 2=roasted beef with no vinegar or lemon. 3=roasted beef after marinating with either vinegar or lemon for 1 hour.

Consuming raw fats such as sesame, coconut, avocado, flax seed and olive oil help to reduce HbA1c. Esposito et al. found that a low carb Mediterranean diet effectively reduced HbA1c, achieved diabetes remission, and delayed the need for medications (11). Harokopio at the University of Athens found eating plenty of olive oil, fish, and whole grains was more effective at slowing the progression of T2DM than a low fat diet. The key factor in the Mediterranean diet is that more than 30% of daily calories are from fat. Olive oil is high in oleic acid and monounsaturated content providing antioxidant and anti-inflammatory properties (12).

Mind body medicine, recognized by the National Center for Complementary Medicine, includes, yoga, Tai Chi, and meditation. These techniques are used to influence the mind body connection. Movement, breathing, meditation, and chanting can be used to achieve life style changes, stress relief, and allow inner focus. The American Diabetic Association recommends 150 minutes a week of moderate to intense physical activity; these mind body activities can be considered moderate exercise. No real improvement in glycemic control was seen but beneficial effects on behavior, mood, stress, and quality of life were identified as positive outcomes (9). Because chronic stress has been implicated as an increased risk factor for the development of T2DM and we know stress induced inflammatory cytokines could be the cause of this finding, it is easy to see how daily practice of mind body medicine would have a positive effect. Many improvements have been documented with daily yoga training. Reduced fasting blood sugar and post-prandial levels, better glycemic control, and stable autonomic control are possible with daily yoga training.

Supplementation

Nutritional supplementation has been effective with diabetes management. As mentioned above various antioxidants are beneficial in preventing complications related to diabetes. The goal is to attempt to include as many fresh nutrient dense ingredients as possible and supplement as needed. High levels of oxidative stress have been found in diabetic patients, increasing the need for antioxidant supplementation. Deficient levels of vitamin C in diabetic patients are compounded by an impaired cellular uptake promoting hyperglycemia, which further decreases intracellular vitamin C levels. This localized deficiency contributes to end organ damage. Vitamin C supplements given at 1000 mg daily decreased urinary albumin and slowed the progression of diabetic nephropathy.

Electrolyte disorders have been found to play an important role in the complications of diabetes and are associated with increased mortality and morbidity. Several factors affect the bodies ability to utilize nutrients including; nutritional status, absorption, acid base imbalances, pharmacokinetics, renal disease, and acute illness. This might explain why diabetic patients are found to be low in several important nutrients. Hypomagnesaemia is commonly identified in diabetic patients. Magnesium is involved with more than 300 enzymatic reactions and is vital to glucose metabolism and insulin homeostasis. Low serum and plasma levels of magnesium are associated with alterations in nerve, muscle, and cardiac conduction. This contributes to nephropathy and end stage renal disease. Increased dietary intake of magnesium improved metabolic control and reduced the risk of T2DM and dyslipidemia (4).

The trace element chromium aids glucose with transport into the cell. Chromium deficiency induces hyperglycemia and impaired glucose tolerance. Normal chromium intake is <20 ug/day. Diet recall was used to determine the daily dietary intake of chromium. Low daily intake led to supplementing with 200 ug chromium picolinate or chromium rich yeast, which resulted in improved glucose tolerance. The findings held true in cases of gestational diabetes as well. Chromium is found in whole grains, broccoli, and grapes. Normal dietary intake ranges from 20-35ug/day, based on sex and age. Reduced HbA1c and fasting blood sugar levels were achieved with chromium supplementation. A large meta-analysis confirmed these results with a combination therapy of 600 ug chromium picolinide and 2 mg biotin (4).

Biotin is a B vitamin that enhances chromium absorption and is involved with intracellular metabolism of glucose. Biotin administration of 9-16 mg/day improved glucose tolerance and decreased mean fasting blood sugar by 45% (4). Inositol, D-chiro-Inositol and D-pinitol are found naturally in legumes and citrus fruits. D-pinitol mediates the action of insulin. When given at 20 mg/kg of body weight, a 5% decrease in plasma glucose is seen (4). Vitamin D deficiency has been associated with increased glucose tolerance and diabetes. Supplementation has shown improvement in endothelial function, glucose tolerance, and an increase in insulin secretion. Doses varied from 800- 300,000 IU/day (4).

a-Lipoic acid (ALA) is an antioxidant. One of its many benefits includes helping to avoid vitamin C and E deficiency which are important to prevent and treat T2DM. Supplementing with 600 mg of alpha lipoic acid effectively increased insulin sensitivity, slowed the progression of complications, and prevented renal damage in T2DM patients. ALA is naturally occurring in broccoli, brussel sprouts, peas, potatoes, and yeast (4).

Herbal Preparations

Bitter melon (momordica charantia) is a plant native to India and Asia. It has been used medicinally for over 600 years. Evidence has shown positive effects on glucose levels, glucose uptake, and glycogen synthesis and glucose oxidation (13). Active ingredients include charantin, vicine, and polypetide-p. Doses ranged from 150 and 2000 mg daily. Fruit, juice, and seed extracts were also used in some studies (12). Minimal side effects have been reported, although the ingredients are contraindicated in pregnancy. Four specific compounds identified provide the biological evidence for the benefits witnessed. An example of traditional or complementary medicine providing new and effective treatments for T2DM is metformin, which originated from goats rue (Galega Officinalis). Tan et al. identified bitter melon as one of the most popular botanical treatments for T2DM (14).

Another promising biologic T2DM treatment is Fenugreek, Trigonella foenum-graecum. Commonly used in Traditional Chinese medicine for glucose control, digestive aid, and relief of menopausal symptoms, Fenugreek given at 100 mg improved fasting blood glucose levels. Fifteen grams of ground fenugreek seed power with a meal lowered postprandial glucose levels (4).

Small trials have yielded promising results for Gymnema sylvestre or gurmar . The leaves of this plant are used in Ayurveda medicine to treat DM, cholesterol, and obesity. Significant improvement in fasting blood sugar and HbA1c levels were obtained with doses from 200 mg to 800 mg of an extract daily (4).

Cinnamon, Cinamonum cassia, gui zhi, Traditional Chinese Medicine, this differs from the common spice Cinnamonum verum. C cassia has been used for thousands of years to treat DM. The herb activates insulin receptors and increases glycogen synthesis. Five clinical trials evaluated doses from 1 – 6 grams daily and saw decreases in fasting blood glucose levels from 18 – 29 % (4).

Red Korean Ginseng was found to improve glucose tolerance test results, fasting plasma glucose, and blood sugar levels. American ginseng (AG) along with an herb called Konjac-Mannan (KJM) may improve T2DM control and associated complications. KJM affects the nutrient absorption rate in the small bowel while AG affects the post absorption activity, they work in unison to increase sensitivity and enhance secretion. Doses ranged from 100 – 200 mg BID reductions in fasting plasma glucose and HbA1c were documented (15).

Berberine is a compound found in golden seal, Oregon grape, barberry, and other plants. Some research as shown it to be as effective as metformin (16). Doses up to 1000 mg twice daily along with life style modifications lead to a 7% reduction in HbA1c. Glucose and lipid lowering properties were identified. Future T2DM treatment may have been identified by targeting free fatty acid metabolism.

Publication trends in Iranian endocrinology outlined highly cited articles effective in treating T2DM. Of the 44 articles found in PubMed, Scopas, and Google Scholar, a few of the relative topics include silybummarianum, Gaertn silyonarin, or milk thistle, as an effective treatment for T2DM and decreased serum glucose and HbA1c levels in diabetic outpatients using psyllium (4).

Shenyan Kangfu, based on Traditional Chinese Medicine and Zhao Enjian’s valuable therapeutic knowledge, is a traditional herbal preparation that has been improved and formulated into tablets. SYKFT tablets consist of 11 herbal ingredients with a synergic effect to nourish the kidney and spleen by detoxifying the body. Widely acclaimed shenya kangfu, has been used for DM nephropathy based on the qi-yin deficiency syndrome; swelling, fatigue, and weak limbs (25). Five sites in four major cities in mainland China have been identified. Enrollment is planned for 80 patients in stage III or IV diabetic nephropathy. Enrollment began in November 2012, 20 participants had been enrolled by March 2013 (17).

As outlined, there are many alternative treatments for T2DM that have been recognized as safe and effective. Small trials, meta-analyses, and anecdotal evidence provide recommendations and document safety concerns while outlining the need for additional research to improve the care that clinicians provide. The Natural Medicine Comprehensive Database confirms that many treatments outlined in this article are safe and effective. The U.S. Department of Health and Human Services contends that there is no high-quality evidence of benefit from alternative or supplemental treatments for diabetes. We as health care providers must use good judgment and available evidence to offer patients the best options for maintaining optimum health. Chandra and associates make it clear that we will never have absolute clarity on which therapies are effective and which are not. So much depends on patient preferences and available alternatives. He calls this the “gray zone” of medicine (18).

Chelation Therapy

Perhaps the most promising advance for the treatment of diabetes since insulin came from the Trial to Assess Chelation Therapy (TACT) (19). This trial emerged from a hearing of the Oversight committee of Congress and a subsequent call for proposals by the National Institutes of Health. TACT was designed to determine if future cardiac events could be reduced for patients at least 50 years of age who had already suffered at least one heart attack. It was a randomized, double-blind, clinical trial of 1708 patients, who were given more than 55,000 intravenous treatments. Half of the patients were given high dose vitamins. Thus there were four groups in the study: double placebo, high dose vitamins without chelation, chelation with placebo vitamins, and chelation with high dose vitamins (20). All of the patients were given evidence-based conventional care for their coronary artery disease. At the beginning of the five years that patients were followed, they were given 30 weekly IV’s and then 10 more treatments at monthly intervals.

The benefit of EDTA chelation was shown to be statistically significant. All of the cardiac events (death, re-infarction, stroke, coronary artery revascularization, and hospitalization for severe angina) were less in the EDTA groups than in the groups that received IV placebos. All cause mortality was also less in the treated patients. Further analysis showed that 37% of the patients had diabetes (322 EDTA and 311 placebo). For those patients with diabetes, there was a 41% reduction in cardiac events, a 52% drop in recurrent MI, and a 43% reduction in deaths. Those who received both chelation and high-dose vitamins had the best results, but even with chelation and placebo vitamins, the NNT for major cardiac events for diabetic patients over the 5 years was 6.5. For statins in such patients the NNT is considered to be highly effective at 17. Chelation was shown to be extremely safe when given according to protocol (18).

A major action of EDTA chelation is its removal of toxic heavy metals, such as lead, cadmium, arsenic, and mercury. Such metals are proven to be toxic to the vascular tree by their free radical activity (21). Carlos Lamar published numerous case studies in the mid-to-late1960 on chelation’s positive effects for diabetes (22). Paul Cutler found significant improvement in diabetic control with the use of the iron chelator, desferoxamine, in diabetic patients who also had high ferritin levels (23). EDTA also chelates iron, but not as effectively as desferoxamine. Therapeutic phlebotomies are more effective than either desferoxamine or EDTA. The vast majority of studies on chelation therapy and vascular disease were not randomized clinical trials and were of insufficient power to draw conclusions. Most of the studies did not identify patients who had diabetes.

The authors of TACT state that the magnitude of benefit for diabetic patients, calls for urgency to replicate their study (24). TACT-2 has been planned. At the same time, other forms of vascular disease, especially peripheral vascular disease, should be studied. Hancke and Flytlie published a remarkable study demonstrating that 24 out of 27 patients on the waiting list for amputation were able to cancel their surgery and save their legs (25).

Patient Decision-Making

In the meantime, TACT is clearly the best evidence available showing that chelation therapy might benefit vascular disease. The new guidelines for vascular problems call for the treating physician to have a conversation with his or her patients explaining the risks and potential benefits of all options of therapy. Then it is imperative that the patient decides what mode of therapy sounds best to him or her. This is the new “gold standard” (26). The patient is the decision-maker, not the doctor. Chelation therapy should be discussed in light of the evidence of TACT. If TACT-2 replicates TACT-1, chelation might be suggested for all diabetic patients. With the current status of evidence, chelation therapy should be offered to patients as an option for treatment, especially if they have signs of vascular disease.

Physicians trained in providing intravenous chelation report better overall results than TACT (27). One reason that clinical practice might be better is that continued monthly maintenance is commonly offered after the basic course of treatment. TACT treated patients intravenously only for the first 20 months, but followed them for 5 years. Another reason could be that TACT did not follow patients with challenge tests for heavy metals or vascular testing to assess progressive improvement. A re-accumulation of toxic metals is not unlikely. Finally, other nutritional therapies are often added by integrative physicians. All of these measures contribute to the best care for each individual patient and would likely improve the overall results.

Chelation therapy has been opposed by many conventional doctors for many years. In 1980, the AMA effectively said to the chelation community, “Put up some evidence, or stop doing the therapy”. With the help of NIH funding and cooperation among doctors familiar with the therapy and a group of courageous cardiologists, the evidence has arrived. As clinical scientists who continually advocate evidence-based medicine, physicians are obligated to accept good evidence when it conflicts with their beliefs (28). The rest of this article puts forth a comprehensive approach to diabetic patients that includes chelation therapy and alternative medicine as therapeutic options for prevention, control of the disease, avoidance of complications, and a longer lifespan.

A Comprehensive Integrative Approach to Diabetes

First, patients must realize it when they have either pre-diabetes or diabetes. This requires screening tests by their doctors’ orders or at health fairs, especially for anyone who is overweight or has a family history of diabetes. Patients with hypoglycemia not infrequently convert to diabetes as they grow older. Fasting blood sugars are a reasonable start but HbA1C tests are more accurate. Those who are overweight should be encouraged to eat less and better, and exercise more. Obesity is a major cause of gene expression into active diabetes.

As soon as pre-diabetes or diabetes is detected, a careful reassessment of lifestyle factors should be instituted. The patient and the family must embrace responsibility for controlling the disease. A healthy diet is crucial, with a special emphasis on low carbs if high triglycerides or the metabolic syndrome is present. Regular exercise and an effective way to deal with stress are important. Smoking and excessive environmental pollution are to be avoided as much as possible. Regular monitoring of lipids, HbA1C, kidney function tests such as creatinine with GFR and micro-albumen, vitamin D3 levels, annual eye exams, vascular screenings, and careful attention to the feet are all required. The sensitive CRP, homocysteine, and ferritin levels should be checked at least once. A challenge test is the best way to screen for toxic metals.

Nutritional supplements can help control the disease and avoid complications. Vitamin C, biotin, chromium, magnesium, zinc, selenium, B-complex, inositol, and alpha lipoic acid should all be considered. Several herbal supplements could also be selected if further control of the blood sugar is needed. Good candidates include cinnamon, bitter melon, and berberine. Fenugreek, Gymnema Sylvestre, Korean or American ginseng, KJM, and combinations of herbs from India or China also might have therapeutic benefit. Milk thistle might help by its detoxification of harmful chemicals. Psyllium is also good for detox, and aids constipation. Generally, herbals are safer and less likely to cause hypoglycemia than medications.

Medications are next on the list. Oral medicines are discussed above, and insulin is a reasonable choice if needed, whether or not the patient is insulin dependent. Doctors must be careful to avoid over-medication that can lead to HbA1C readings that are too low, hypoglycemic episodes, and severe injuries, especially in the frail elderly. Control of the disease is imperative. Therapeutic goals for the HbA1C should be 6.5-7.0 for most patients and 8.0 for unstable elderly patients. Of course, lower levels of HbA1C are desirable if they are achieved without the help of medications.

The most dramatic evidence of treatment success in the last few years came with TACT. Chelation therapy reduced future cardiac events and lowered the death rate for patients with diabetes who had a previous myocardial infarction. The magnitude of benefit was perhaps greater than any intervention other than considerable weight loss or insulin therapy. The probable mechanism has to do with free-radical activity and inflammation caused by toxic metals, which are removed with chelation. Confirmatory research is coming with TACT-2, but cardiologists and endocrinologists should at least describe the remarkable evidence generated by TACT-1 and let patients choose whether they want chelation, either before or after significant vascular disease has developed. After all, most of the complications from diabetes are vascular, which can lead to devastating disabilities and/or premature death.

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