Oral Chelation Or IV Chelation To Improve Bone Density

Q. Dear Dr. Dean,

I am a 58-year old healthcare professional currently working on a postgraduate degree. With a few exceptions, I believe I am in very good health. I had a thyroidectomy 13 years ago for thyroid cancer. I was over-treated with levothyroxine for 12 years, which decreased my bone density substantially. In 2006, I had a complete abdominal hysterectomy due to adenomyosis (a benign condition characterized by ingrowth of the endometrium into the uterine musculature). I had a severe leg fracture two years ago (due to osteoporosis), and had to spend several weeks in a non-weight bearing position. My dexa scan reported a T-Score of –4.2!

I’ve consequently herniated and/or ruptured up to 12 discs in my spine. I am undergoing prolozone therapy for that, and it is helping. I have purchased an ozone machine and am ingesting ozonated water two times a day and doing vaginal insufflation 2 to 3 times a week.

I also do gentle walking and other movements on a PowerPlate 2 to 3 times a week.

One of my doctors wants me to undergo EDTA chelation to improve my bone density. He claims that it would be faster than taking oral chelation products. What is your opinion regarding suppository chelation as another alternative? I have read the numerous studies that are available online on the pros and cons. I would appreciate your advice.

KATHY, Pipersville, PA

Dear Kathy,

A. T-Score of –4.2 indicates that you are indeed at high risk for new fractures (Fig. 1).

With regard to your question about chelation, I want to qualify my answer. I’m a proponent of chelation therapy (IV and oral). I’ve administered chelation therapy to my patients since 1985, and I‘ve witnessed a number of “miraculous” effects of chelation on a number of chronic degenerative conditions. I continue to be amazed at the benefits of chelation.

Figure 1. A bone density scan gives a T-score that determines one’s risk for fractures. A T-score compares one’s bone density to the bone density of a healthy, young adult woman. A T-score of –2.5 or lower is defined as osteoporosis. The lower the score, the greater the fracture risk.
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Nevertheless, I don’t recommend chelation as a primary modality to treat your osteoporosis. Chelation proponents have for years theorized about the effects of chelation on calcium metabolism and bone density. When EDTA is infused into the body, there is a temporary drop in serum calcium, and an increase in parathormone levels. This is believed to release metastatic calcium from stores in the body where it doesn’t belong (arterial intima, arthritic joints, calcified valves, etc.), and to stimulate the formation of osteoblasts (cells associated with the production of bone), which should result in enhancement of bone density, and reversal of osteoporosis.

The problem was that there had been no studies to confirm this hypothesis. In 1988, physicians at the McDonaugh Medical Center in Missouri, conducted a study to answer the question: Does EDTA therapy have a positive or negative effect on bone density?1 They enrolled 61 patients in their study (23 males, 38 females), whose average age was 65. Bone density was evaluated using a now-obsolete single photobone densitometer manufactured by Norland (Although this instrument is no longer used, it provided results that were known to be accurate).

After three months of treatment with over 30 chelations, there was a slight, non-significant increase in bone density in the entire group. However, when the data for 25 of the patients who were diagnosed as having osteoporosis was separated out from the group as a whole, the post-treatment results showed a modest increased bone density of about 2%.

The authors concluded that, “EDTA therapy might enhance bone growth in patients with osteoporosis and has no negative effect on patients with normal bone density readings.” Nevertheless, this result for osteoporosis pales when compared to the dramatic benefits of EDTA chelation for cardiovascular disease (i.e., I had a recent patient whose more than 60% blockage of his carotid arteries was reduced to less than 30% after receiving more than 30 treatments). Chelation may help osteoporosis — and it certainly won’t hurt — but it is not a silver bullet.

Figure 2. Rate of absorption of orally administered EDTA, as determined by fecal recovery from 3 healthy subjects.2
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With regard to the other half of your question, regarding oral versus rectal suppositories of EDTA, I do not recommend the suppositories. Oral EDTA is admittedly poorly absorbed (see Fig. 2) — perhaps a maximum of 10% is systemically absorbed and excreted via the kidneys. The remainder passes unchanged through the gastrointestinal tract, where it is excreted unchanged in the stool.2 Thus, since there is such minimal absorption of oral EDTA during its transit through the entire gastrointestinal tract, oral EDTA will wind up in the rectum. I don’t believe one will benefit more from EDTA suppositories inserted per rectum than one would benefit by consuming EDTA orally, and enabling it to transit the entire GI tract.

Oral EDTA may be used in conjunction with the intravenous treatment. I recommend both oral and IV treatments for maximum efficacy. Intravenous EDTA is administered over a short time — 30 minutes to 3 hours — once or twice per week. Virtually all of it is excreted via the kidneys within 24 hours. With daily consumption of oral EDTA, fairly low doses are in the blood, but these levels are there every day. Consumption of 1,000 mg of oral EDTA each day, with absorption of about 10%, is like having one additional intravenous treatment spread over a month.

There are a number of other things that you can do to enhance your bone density, in addition to what you are doing.

Dehydroepiandrosterone (DHEA)

Figure 3. Decline of DHEA-S with age.3
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DHEA is the most abundant steroid hormone in the body, and drops predictably with age in men and women (see Fig. 3).3 DHEA supplementation has been reported in a number of studies to have positive effects on bone density and reversal of osteoporosis.4,5 I recommend starting with 25 mg DHEA (50 mg for men), first thing in the morning, as that is when DHEA levels are highest (peak is from 4–8 AM). The dosage can be titrated up or down depending on the response. Testosterone is the dose-limiter for women, who very efficiently convert DHEA into testosterone. If facial hair or acne develops, reduce the dose.


Xylitol is a five-carbon sugar that has a number of unique properties. It looks like sugar, tastes like sugar, and is heat-stable (so it can be used in baked goods). Xylitol does not cause significant changes in blood glucose or insulin (making it safe for diabetics and those trying to lose weight, but also for those who understand the importance of maintaining low levels of glucose and insulin as part of an anti-aging regimen).

Osteoporosis is another condition for which xylitol may be of help. Scientists in Finland showed that xylitol was able to maintain bone density in rats which had their ovaries surgically removed.6 Without ovaries, estrogen levels in these rats plummeted — and so did the bone density in the rats which were not given xylitol. However, in ovariectomized rats that had been given xylitol, bone density actually increased.

This early study strongly indicated that xylitol might help maintain bone density in normally aging animals. Subsequent studies confirmed this conjecture. A later report by the same team of Finnish scientists evaluated the effect of xylitol on bone volume and bone mineral content in aged male rats, reinforcing their earlier study on female animals.7

In this later study, 24 rats were given xylitol in their diet for twenty months. At the end of this time, they were “euthanized” with carbon dioxide, and the bone mineral content and volume of the bones was evaluated by several sophisticated analytical techniques.

The tibial (lower leg bone) density of control animals averaged 1.560 g/mm3, while the density of the tibias of the xylitol-fed animals averaged 1.725 g/mm3, indicating a xylitol-induced increase of bone density of nearly 10%. The authors stated that “Xylitol consumption resulted in significant protection against aging-related loss of bone,” and “The preserved bone volume indicates an anabolic and/or anti-catabolic effect … caused by Xylitol.” They concluded: “A continuous moderate dietary xylitol supplementation leads to an increased bone volume and to an increased bone mineral content in the long bones of aged rats. This indicates a xylitol-induced protection against aging-related osteoporotic changes.”

In a rare action for academic scientists, the Finnish researchers made bold recommendations for human application of their studies. Based on their study with rats (the rats were given about two grams of xylitol daily — 7% of their daily caloric intake), the scientists extrapolated that a human dose would be about 40 grams daily (many people routinely take 30 to 60 grams of xylitol per day). Xylitol does not appear to have a toxic dose. People have safely taken doses as high as 400 grams daily for prolonged periods without significant ill effects (initially, such high doses may cause diarrhea).


Strontium has been safely used as a medicinal substance for more than an hundred years. It was first listed in Squire’s Companion to the British Pharmacopeia in 1884. Subsequently, strontium was used therapeutically in the United States and Europe. As late as 1955, strontium compounds were still listed in the Dispensatory of the United States of America. In the first half of the twentieth century, strontium salts were administered in dosages of 200–400 mg/day without toxic effects.

In 1959, researchers at the Mayo Clinic investigated the effect of strontium in 32 individuals suffering from osteoporosis.8 Each patient received 1.7 grams of strontium per day as strontium lactate. Eighty-four percent of the patients reported marked relief of bone pain, and the remaining 16 percent experienced moderate improvement. No significant side effects were seen, even with prolonged (up to three years) administration of strontium. X-rays taken at the beginning and end of the study showed “probable” increased bone mass in 78 percent of the cases. This is not surprising, considering the symptomatic improvement reported by the patients. Unfortunately, measurement of bone mass in 1959 was pretty crude, leading the researchers to qualify their interpretation of the X-rays. Sophisticated tests such as dual photon absorptiometry and CT scanning as used today were not available at the time this study was conducted.

In 1985, Dr. Stanley C. Skoryna of McGill University in Montreal conducted a small-scale study that pointed to a potential role for strontium in the treatment of humans.9 Three men and three women with osteoporosis were each given 600 to 700 mg per day of strontium as strontium carbonate. Bone biopsies at the iliac crest (hip bone), before and after six months of treatment, showed a 172 percent increase in the rate of bone formation after strontium therapy, with no change in bone resorption. The patients receiving strontium remarked that the pains in their bones had diminished and their ability to move around had improved.

Recently, interest in strontium has been rekindled by a number of studies using the strontium salt of ranelic acid (strontium ranelate). A large multi-center trial investigated the efficacy and safety of different doses of strontium in the treatment of postmenopausal osteoporosis.10

Figure 4. Increase in lumbar bone mineral density after two years treatment with strontium in doses of 170, 340, and 680 mg/day.11
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The study included 353 osteoporotic women with at least one previous vertebral fracture and low scores of lumbar bone density. Patients received placebo or strontium in doses of 170, 340 or 680 mg per day for two years. Lumbar and hip bone mineral density (BMD) were measured using dual-energy X-ray absorptiometry (DXA), and the investigators also determined the incidence of new vertebral fractures, as well as several biochemical markers of bone metabolism. Lumbar BMD increased in a dose-dependent manner as shown in Fig. 4.

There was a significant reduction in the number of patients with new vertebral fractures in the second year of the group receiving the 680 mg per day dose, and there was also a significant positive change in markers of bone metabolism. The authors concluded that 680 mg per day of strontium offered the best combination of efficacy and safety, and stated without equivocation that “strontium therapy increased vertebral BMD and reduced the incidence of vertebral fractures.”

A much larger trial by the same research team included 1,649 osteoporotic postmenopausal women, who received 2 grams per day of strontium ranelate (providing 680 mg strontium) or placebo for three years.12 Calcium and vitamin D supplements were also given to both groups before and during the study. Patients in the strontium group suffered fewer fractures, increased lumbar bone mineral density by an average of 14.4 percent, and femoral neck BMD an average of 8.3 percent. The authors concluded “treatment of postmenopausal osteoporosis with strontium ranelate leads to early and sustained reductions in the risk of vertebral fractures.”

One of the largest studies on strontium ranelate, published in the January 30, 2006 online addition of the journal Bone, investigated its effects on more than 7,000 postmenopausal women with osteoporosis.13 After one year and three years, strontium ranelate proved significantly effective as an antifracture agent compared with placebo in patients with prevalent vertebral fracture. After one year, the risk of new vertebral fractures was reduced by 49 percent and after three years, by 41 percent in women taking the strontium ranelate. In addition, the relative risk of clinical vertebral fracture was significantly reduced by 52 percent after 1 year and by 38 percent over 3 years in the strontium ranelate group compared with placebo. Strontium ranelate also significantly decreased the relative risk of vertebral fractures by 45 percent in patients without prevalent vertebral fracture over 3 years compared to placebo. Bone mineral density also was increased during 3 years of treatment with strontium ranelate in comparison with placebo.

According to the study authors, “Strontium ranelate, 2 grams per day orally (680 mg of strontium), is a new, effective, and safe treatment for postmenopausal patients with osteoporosis, to reduce the vertebral fracture risk in patients with or without a history of vertebral fracture.”

Although the more recent studies used strontium ranelate, earlier studies used other salts of strontium, including strontium carbonate, strontium lactate, and strontium gluconate. It appears that the active ingredient is strontium, and whatever salt of strontium used is less important than the amount of strontium consumed.14

Doses of 680 mg per day appear to be the optimum dose, although lower doses are clinically effective. Dr. J.Y. Reginster (2002), one of the principal strontium researchers, cautions that co-administration of strontium with calcium appears to impair strontium absorption,15 so I recommend that strontium be taken on an empty stomach, and that it especially not be taken at the same time as other multi-minerals that usually include calcium.


Figure 5. Typical bone mineral density (BMD) changes with Progesterone (P), Estrogen only (E), and Control (C). In this graph, it can be seen that the untreated postmenopausal patient with osteoporosis will lose 1.5% bone mass per year; that estrogen supplementation will tend to maintain bone mass; but only the addition of natural progesterone will increase bone mass, thus reversing the osteoporotic process.18
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Dr. John Lee has, since 1982, treated postmenopausal osteoporosis with transdermal natural progesterone, and demonstrated true reversal of osteoporosis in patients who did not use estrogen supplements.15–17 Figure 5 illustrates the typical difference in bone mineral density (BMD) changes over a three year period between a group of 63 patients using progesterone supplementation, compared to the typical effect of estrogen treatment, and natural course of untreated controls.18 I usually recommend 20–40 mg of topical progesterone per day, although the dosage and treatment regimens vary based on the patient’s response.

Good luck with your bone-building program. Please let me know how you do,

Ward Dean, MD


  1. Rudolph CJ, McDopnagh EW, Wussow DG. The effect of intravenous disodium ethylenediaminetetraacetic acid (EDTA) upon bone density levels. J Adv Med. 1988;1:79–84.
  2. Foreman H, Trujillo T. The metabolism of C14 labeled ethylenediaminetetraacetic acid in human beings. J Lab Clin Med. 1954[43:566–71.
  3. Finch CE, Mobbs CV. Nonlethal measurement involving steroids and neurotransmitters as reflections of physiological aging. In: Reff ME, Schneider EL, editors. Biological Markers of Aging (NIH Publication No. 82–2221). Washington, DC: U.S. Government Printing Office; April, 1982. p.30–41.
  4. Samaras N1, Samaras D, Frangos E, et al. A Review of Age-Related Dehydroepiandrosterone Decline and Its Association with Well-Known Geriatric Syndromes: Is Treatment Beneficial? Rejuvenation Res. 2013 Aug;16(4):285–94.
  5. Papierska L, Rabijewski M, Kasperlik-Załuska A, Zgliczy´nski W. Effect of DHEA supplementation on serum IGF-1, osteocalcin, and bone mineral density in postmenopausal, glucocorticoid-treated women. Adv Med Sci. 2012 Jun 1;57(1):51–7.
  6. Svanberg, M, Knuuttila, M. Dietary xylitol prevents ovariectomy induced changes of bone inorganic fraction in rats. Bone Miner. 1994 Jul;26(1):81–8.
  7. Mattila PT, Svanberg MJ, Knuuttila ML. Increased bone volume and bone mineral content in xylitol-fed aged rats. Gerontology. 2001 Nov-Dec;47(6):300–5.
  8. McCaslin FE Jr, Janes JM. The effect of strontium lactate in the treatment of osteoporosis. Proc Staff Meetings Mayo Clin. 1959;34:329–34.
  9. Marie PJ., Skoryna SC, Pivon RJ, et al. Histomorphometry of bone changes in stable strontium therapy. In: Hemphill DD, editor. Trace substances in environmental health XIX. Columbia, Missouri: University of Missouri; 1985. p.193–208.
  10. Meunier PJ, Slosman, DO, Delmas PD, et al. Strontium ranelate: dose-dependent effects in established postmenopausal vertebral osteoporosis — a 2-year randomized placebo controlled trial. J Clin Endocrinol Metab. May 2002;87(5):2060–6.
  11. Meunier PJ, Roux C, Seeman E, et al. The effects of strontium ranelate on the risk of vertebral fracture in women with postmenopausal osteoporosis. N Engl J Med. 2004, Jan 29;350(5):459–68.
  12. Ortolani S, Vai S. Strontium ranelate: An increased bone quality leading to vertebral antifracture efficacy at all stages. Bone. 2006 Jan 30;38(2S1):19–22.
  13. Skoryna SC. Effects of oral supplementation with stable strontium. Can Med Assoc J. 1981 Oct 1;125(7):703–12.
  14. Reginster JY, Deroisy R, Dougados M, Jupsin I, Colette J, Roux C. Prevention of early postmenopausal bone loss by strontium ranelate: the randomized, two-year, double-masked, dose-ranging, placebo-controlled PREVOS trial. Osteoporos Int. 2002 Dec;13(12):925–31.
  15. Lee JR. Osteoporosis reversal: The role of progesterone. Intern Clin Nutr Rev. 1990;336, (8726):1327.
  16. Lee JR. Osteoporosis reversal with transdermal progesterone (letter). Lancet. 1990; 336:1327.
  17. Lee JR. Is natural progesterone the missing link in osteoporosis prevention and treatment? Medical Hypotheses. 1991;35:316–8.
  18. Lee JR. Natural Progesterone — The multiple roles of a remarkable hormone. Sebastopol, CA: BLL Publishing, 1995.

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