Fortune Article

Scientific Problem Cancer is a group of over 100 diseases and unlike normal cells, the cells in cancers change the three-billion-letter DNA code when they replicate. This is a major obstacle.
Download a copy of Why we’re Losing The War On Cancer and How to Win It! PDF

We are not winning the war on cancer

War on Cancer
In 1971 Nixon initiated a major war on cancer. The industry feuded over how centralized of a role the government should have and how the money should be spent.
Sidney Farber, the Boston physician known as the godfather of cancer research did not want to wait for the industry to academically understand the complicated workings of cancer, rather he wanted to get busy treating people even if the methods used would not be fully understood.
Dr. Farber who wanted a government controlled unified assault on cancer, testified in 1971 congressional hearings that…

Farber lost.
Since 1971 we have wasted billions on trying to understand the diseases and getting useless cancer drugs approved before they can be used, loosing over 1500 people per day!
This has been a highly profitable business for both researchers and the patent-drug
corporations. However this has not created any benefits for the sick because this kind of a
for profit system will only reward those taking minimum risk; finding tiny improvements in
a far distant corner of the cancer world. When scientists are asked what they think of this
system they talk of “dysfunctional cancer culture”

The Money

The Mouse
It has been known for one or two decades that preclinical human cancer models have very
little predictive power in terms of how actual human tumors, inside patents, will respond.
So the tumors that arise in each, with the same flip of a genetic switch, are vastly different.
Says Weinberg: “ A fundamental problem with remains to be solved in the whole cancer
research effort, in terms of therapies, is that the preclinical models of human cancer, in large
part, stink”
As explained by Bruce Chabner, professor of medicine at Harvard and clinical director at the
Massachusetts General Hospital Cancer Center: the “instant tumors” that researchers cause
in miche simply can’t mimic human cancer’s most critical and maddening trait, its quick
changing DNA.
Homer Pearce, former cancer research and clinical investigator at Eli Lilly and is now
research fellow at the drug company agrees that mouse models are “woefully inadequate”
for determining whether a drug will work in humans: If you look at the millions and
millions and millions of mice that have been cured, and you compare that to the relative
success, or lack thereof, that we’ve achieved in the treatment of metastatic disease
clinically” he says, “you realize that there just has to be something wrong with those models.
Vishva Dixit, a VP for research in molecular oncology at Genentech in South San Francisco,
is even more horrified that “99% of investigators in industry and in academia use
xenografts.” Why is the mouse model so heavily used? Simple. “it is very convenient, easily
manipulated, “Dixit explains. “You can assess tumor size just by looking at it.”
If everyone understands the problem, why isn’t anything being done?
Two reasons, says Weinberg. First, there’s no other model with which to replace the
poor mouse. Second, he says, “is that the FDA has created inertia because it continues to
recognize these [models] as the gold standard for predicting the utility of drugs.”
It is not localized tumors that kill people with cancer; it is the process of metastasis – and
incredible 90% of the time. Aggressive cells spread to the bones, liver, lungs, brain, or other
vital areas, wreaking havoc.
NCI grants going back to 1972 show that less than 0.5% of study proposals focused
primarily on metastasis. Of the tens of thousands of grant proposals awarded, over 90%
even don’t mention the word metastasis.
M.D. Anderson’s Josh Fidler suggests that metastasis is getting short shrift simply
because “it’s tough. Okay? And individual are not rewarded for doing tough things.” He
claims grant reviewers are more comfortable with the studies that use antibody on a
specific cancer.
FDA mandate is to make sure that a drug is safe and that it works before allowing its sale
to the public. Thus, the regulators need to see hard data showing that a drug has had some
effect in testing.
However, it’s hard to see “activity” in preventing something from happening in the first
place. There have been little funding in the area so the biomarkers have not been found.
[check Ralph Moss]
Drug companies don’t focus on metastasis (the thing that kills 90% of cancer patients)
instead they focus on shrinking tumors (the thing that kills 10% of cancer pateints).
Those ineffective drugs keep getting approved with FDA. However here as in other cases in
the patent-drug industry, the new drugs are not any better than the new ones – just more
The flawed models for cancer drug development:
Obsession with tumor shrinkage. Focus on cell functions to the near exclusion of what’s
happening in the organisms as a whole.
Clinical trials are so arduous and expensive that it takes 12 to 14 years to develop and over
$800 million.
This rewards companies that spend huge time and vast money on proving that their drugs
work – even if the drug only works a little better than the last one. For example shrinks
tumors 10% better than previous drugs.
No one wants to risk spending over $800 million on a drug that deals with the problem of
metastasis when the rules to get it approved focus more on the science than the cure.
Doctors need the freedom to administer drugs in combination because tumors recruit blood
vessels through several signaling mechanisms, researchers believe, so the best approach is
to apply several drugs, cutting off all routes.
He concludes that we need to move away from “the rules governing drug approval to tort
law and intellectual property rights” and that: “Science now has the knowledge and the
tools; we need to act.”
I agree that we need to move away from FDA rules governing drug approval, but I disagree
that we need to replace those with tort law and intellectual property rights.
Profiteering on cancer, through intellectual property rights, is one of the main hindering
factors to finding the true cure for cancer.
In fact like with many other industries, the solution is already available but suppressed.
The cure for cancer has been made available by a number of immune supporting therapies
for decades. Those methods have been vilified, ridiculed and suppressed by the scientific
If we were in a court of law, arguing a murder case, the evidence would suffice to persuade a
When it comes to curing cancer using lifestyle, food and supplements the burden of proof
becomes overwhelming.
Let me mention an example. Dr. Hulda Clark presented meticulous case histories of over
50 people that she treated for cancer in her book “The Cure for All Advanced Cancers”. The
success rate for advanced cancer is about 95%
Those case histories were supported with before and after x-rays and other medical
information. So you can count on this method, not merely hope it will work for you. It is
a total approach that not only shrinks tumors, but also normalizes your blood chemistry,
lowers your cancer markers, and returns your health. The small failure rate (5%) is due to
clinical emergencies that beset the advanced cancer sufferer. However, if you combine the
advice in this book with access to hospital care, even “hopeless” patients can gain the time
necessary to become well again.
If a jury would be asked to deliberate and decide if cancer can be cured using her methods
and they were given the evidence in the book, I am confident they would rule that Dr. Hulda
Clark did actually cure those people.
However this is not the experience Dr. Clark had when asking an oncologist to testify if the
x-rays and medical information presented indicated a cure of cancer. The doctor simply
asked for a biopsy. He told Dr. Clark that he could not testify that the original series of x-
rays he had in his hands, that clearly indicated a shrinking tumor, indicated that it was in
fact tumor. He needed a biopsy to be conclusive.
The laws governing medical treatment need to be changed to primarily support natural
therapies, that incorporate lifestyle, food and supplements.

Research Findings on CoQ10 Anti-Cancer Role

Human Studies Urgently Needed
By William Faloon
Startling research findings released in 2005 indicate that coenzyme Q10 may have a role in cancer treatment. Not only is there favorable human clinical data, but scientists have also discovered new anti-cancer mechanisms related to CoQ10.
Coenzyme Q10 was first prescribed in Japan to treat heart disease in the 1960s.1 Beginning in the 1990s, scientists hypothesized that CoQ10 may help prevent certain brain diseases. When doctors gave high doses of CoQ10 to Parkinson’s patients, disease progression slowed by 44%.2
Scant attention was paid to a 1994 European study in which breast cancer patients were treated with CoQ10. The result of this European study was tumor regression and improved long-term survival in patients whose cancers had spread too far to be completely removed by surgery.3
CoQ10 is so closely associated with heart and brain function that few people understand its role against cancer. Scientists investigating the effects of CoQ10 have uncovered evidence that CoQ10 can selectively kill cancer cells without harming normal cells—something that conventional chemotherapy cannot do.4,5
Tamoxifen and CoQ10
Tamoxifen is a drug used to treat breast cancer. Its principal mechanism is to block estrogen-receptor sites on cancer cell membranes, thereby reducing the cell-proliferating effects of estrogen. As is typical of anti-cancer drugs, tamoxifen can induce serious side effects.
Scientists sought to find out whether coenzyme Q10 could improve the cell-killing effects of tamoxifen. In a study published in May 2005, rats with mammary tumors were given tamoxifen, coenzyme Q10, tamoxifen plus coenzyme Q10, or no therapy. Compared to rats receiving no therapy, those receiving either CoQ10 or tamoxifen had greatly reduced tumor weight and volume.6
The most significant tumor-suppressing effect, however, was seen in the group receiving tamoxifen plus coenzyme Q10. In this group, there was virtually no increase in tumor weight, while in the untreated group, tumor weight increased more than threefold. The scientists concluded that the addition of CoQ10 increased the susceptibility of cancer cells to tamoxifen.6
In a related study published in February 2005, mammary tumor proliferation in rats was prevented by the administration of tamoxifen plus CoQ10, niacin, and riboflavin.7
Free radicals are involved in the initiation and promotion of cancer.6,8-20 In these recent studies, rats with mammary tumors displayed elevated free radical activity and low levels of natural antioxidants such as SOD, catalase, and glutathione.6,7 The administration of nutrients such as CoQ10 with tamoxifen caused natural antioxidant levels to be greatly restored. The result was significant inhibitory effects on cancer cell proliferation.
Novel Research from the University of Miami
A startling finding of CoQ10’s anti-cancer mechanism of action was discovered in recent studies conducted at the University of Miami’s Leonard M. Miller School of Medicine.21 In a July 2005 telephone interview, principal investigator Dr. S.L. Hsia told Life Extension:
“This is the first time in history we have been able to selectively teach a cancer cell to kill itself with CoQ10, via a mitochondrial mechanism, without harming the healthy cells.”5
According to research director Niven R. Narain, cancer cells lose their apoptotic potential, or ability to respond to programmed cell death, but CoQ10 restores apoptotic potential to cancer cells. Mr. Narain told Life Extension:
“The data suggest that CoQ10 significantly reduces expression of the bcl-2 gene family, which is responsible for conferring resistance to cell death. In essence, CoQ10 modulates bcl-2 in a manner that allows the cancer cell to kill itself without adversely affecting normal cells. This is why we say it is ‘selective,’ because the bcl-2 family is not affected in normal cells.”
Several published animal and human studies have demonstrated CoQ10’s remarkable effects against certain cancers.22-33 The University of Miami research reveals a mechanism to explain why CoQ10 is so lethal to cancer cells, but non-toxic to healthy cells.
NCI Analyzes CoQ10 Data
In early 2005, the National Cancer Institute (NCI) analyzed the scientific literature on coenzyme Q10 and cancer.34
In a published report, the NCI discussed CoQ10’s “immunostimulatory” potential as one reason why it is being used as an adjuvant therapy in cancer patients. The NCI report confirmed CoQ10’s ability to protect against certain types of chemotherapy drug-induced damage to the heart.34-43
The NCI stated that blood levels of coenzyme Q10 are frequently reduced in cancer patients and reported on a successful European study showing 100% survival in breast cancer patients supplementing with 90 mg per day of CoQ10. The NCI report also stated that all breast cancer patients who supplemented with CoQ10 experienced decreased use of painkillers, improved quality of life, and an absence of weight loss.
The NCI next described a follow-up study in which breast cancer patients were treated with higher CoQ10 doses of 300-390 mg/day, and the result was “complete regression of their residual breast tumors.”3
In another small study, the NCI reported on three breast cancer patients who were followed for three to five years while taking high-dose coenzyme Q10 (390 mg/day).44
One patient had complete remission of liver metastases, another had remission of a tumor that had spread to the chest wall, and the third patient had no microscopic evidence of remaining tumor.
In reviewing anecdotal reports appearing in the peer-reviewed scientific literature, the NCI reported that coenzyme Q10 has been shown to lengthen the survival of patients with pancreatic, lung, rectal, colon, and prostate cancers.34
Despite these impressive findings, the NCI pointed out that the human studies showing the anti-cancer effects of CoQ10 have several weaknesses, including the absence of a control group and the fact that these patients were undergoing conventional therapy in addition to taking CoQ10. Thus, according to the NCI, “it is impossible to determine whether any of the beneficial results was directly related to coenzyme Q10 therapy.”45
Please note that the NCI’s report on CoQ10 was published before the impressive University of Miami gene studies and the controlled rat studies showing that CoQ10 enhances the anti-tumor effects of tamoxifen.
Human Studies Urgently Needed
In 2005, more than 200,000 women were diagnosed with invasive breast cancer, and 40,000 died from it.46
Compelling research findings indicate that coenzyme Q10 might be an effective adjuvant therapy.
Drug companies, however, continue to ignore CoQ10. The NCI has plenty of clinical trials planned to test toxic chemotherapy drugs, but has no studies scheduled to evaluate CoQ10’s effects on breast cancer patients. This is regrettable, considering the NCI’s own published report on CoQ10’s potential efficacy. The University of Miami researchers are planning skin, breast, and prostate cancer studies in which CoQ10 will be tested in vitro, in animal models, and in human cancer patients.
Every three minutes, a woman in the United States is diagnosed with breast cancer.47. There is an urgent need to initiate a large clinical study to determine CoQ10’s efficacy in the adjuvant treatment of breast cancer.
Unlike most experimental anti-cancer drugs, CoQ10 is free of toxicity. This means that high doses (400 mg/day) could easily be tested on breast cancer patients and the outcomes assessed in a relatively short time. If coenzyme Q10 is only 25% as effective as preliminary clinical studies indicate, 10,000 women a year could be spared agonizing deaths.
As a member of the Life Extension Foundation, you gain access to groundbreaking research years before the public learns about it. In too many instances, valuable clinical data remains buried in the scientific literature while human beings perish needlessly.
Throughout 2005, the astounding findings about coenzyme Q10 and cancer should have made headline news. Instead, both the media and cancer establishment ignored these remarkable discoveries that could have saved tens of thousands of lives. The fact that the National Cancer Institute has failed to initiate funding to ascertain how effective coenzyme Q10 may be as an adjuvant cancer therapy is a disgrace.
Life Extension members should take comfort in knowing they are part of an organization that seeks to tear down the archaic barriers that deny Americans access to lifesaving therapies. For 26 consecutive years, the Life Extension Foundation has bypassed a bureaucratic labyrinth that separates human beings from the fruits of scientific discovery. I want to thank our growing legion of members for supporting the many programs we have in place to combat age-related disease.
For longer life,
William Faloon
1. Yamaura Y, Ishiyami T, Yamayami T, et al. Clinical use of coenzyme Q for treatment of cardiovascular diseases. Jap Circ. J. 1967;31:168.
2. Shults CW, Oakes D, Kieburtz K,et al. Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline. Arch Neurol. 2002 Oct;59(10):1541-50.
3. Lockwood K, Moesgaard S, Folkers K. Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10. Biochem Biophys Res Commun. 1994 Mar 30;199(3):1504-8.
4. Available at: ma.ultranet/BiologyPages/B/BCL2.html. Accessed November 11, 2005.
5. Available at: Accessed October 31, 2005.
6. Perumal SS, Shanthi P, Sachdanandam P. Combined efficacy of tamoxifen and coenzyme Q10 on the status of lipid peroxidation and antioxidants in DMBA induced breast cancer. Mol Cell Biochem. 2005 May;273(1-2):151-60.
7. Perumal SS, Shanthi P, Sachdanandam P. Augmented efficacy of tamoxifen in rat breast tumorigenesis when gavaged along with riboflavin, niacin, and CoQ10: effects on lipid peroxidation and antioxidants in mitochondria. Chem Biol Interact. 2005 Feb 28;152(1):49-58.
8. Florence TM. The role of free radicals in disease. Aust NZ J Ophthalmol. 1995 Feb;23(1):3-7.
9. Weitzman SA, Turk PW, Milkowski DH, Kozlowski K. Free radical adducts induce alterations in DNA cytosine methylation. Proc Natl Acad Sci USA. 1994 Feb15;91(4): 1261-4.
10. Arikan S, Akcay T, Konukoglu D, Obek C, Kural AR. The relationship between antioxidant enzymes and bladder cancer. Neoplasma. 2005;52(4):314-7.
11. Bhasin G, Kauser H, Athar M. Free radical generating agents lead to the rapid progression of benign skin tumors to carcinoma in iron-overloaded mice. Arch Toxicol. 2004 Mar;78(3):139-46.
12. Athar M. Oxidative stress and experimental carcinogenesis. Indian J Exp Biol. 2002 Jun;40(6):656-67.
13. Pryor WA. Cigarette smoke radicals and the role of free radicals in chemical carcinogenicity. Environ Health Perspect. 1997 Jun;105 Suppl 4:875-82.
14. Borek C. Free-radical processes in multistage carcinogenesis. Free Radic Res Commun. 1991;12-13 Pt 2:745-50.
15. Sun Y. Free radicals, antioxidant enzymes, and carcinogenesis. Free Radic Biol Med. 1990;8(6):583-99.
16. O’Connell JF, Klein-Szanto AJ, DiGiovanni DM, Fries JW, Slaga TJ. Enhanced malignant progression of mouse skin tumors by the free-radical generator benzoyl peroxide. Cancer Res. 1986 Jun;46(6):2863-5.
17. Troll W, Frenkel K, Teebor G. Free oxygen radicals: necessary contributors to tumor promotion and cocarcinogenesis. Princess Takamatsu Symp. 1983;14:207-18.
18. Mates JM, Sanchez-Jimenez FM. Role of reactive oxygen species in apoptosis: implications for cancer therapy. Int J Biochem Cell Biol. 2000 Feb;32(2):157-70.
19. Duthie SJ, Ma A, Ross MA, Collins AR. Antioxidant supplementation decreases oxidative DNA damage in human lymphocytes. Cancer Res. 1996 Mar 15;56(6):1291-5.
20. Weber C, Sejersgard JT, Mortensen SA, Paulsen G, Holmer G. Antioxidative effect of dietary coenzyme Q10 in human blood plasma. Int J Vitam Nutr Res. 1994;64(4):311-5.
21. Available at: Accessed October 31, 2005.
22. Hodges S, Hertz N, Lockwood K, Lister R. CoQ10: could it have a role in cancer management? Biofactors. 1999;9(2-4):365-70.
23. Folkers K, Osterborg A, Nylander M, Morita M, Mellstedt H. Activities of vitamin Q10 in animal models and a serious deficiency in patients with cancer. Biochem Biophys Res Commun. 1997 May 19;234(2):296-9.
24. Folkers K, Brown R, Judy WV, Morita M. Survival of cancer patients on therapy with coenzyme Q10. Biochem Biophys Res Commun. 1993 Apr 15;192(1):241-5.
25. Lockwood K, Moesgaard S, Hanioka T, Folkers K. Apparent partial remission of breast cancer in ‘high risk’ patients supplemented with nutritional antioxidants, essential fatty acids and coenzyme Q10. Mol Aspects Med. 1994;15 Suppls231-s40.
26. Bliznakov EG. Effect of stimulation of the host defense system by coenzyme Q 10 on dibenzpyrene-induced tumors and infection with Friend leukemia virus in mice. Proc Natl Acad Sci USA. 1973 Feb;70(2):390-4.
27. Perumal SS, Shanthi P, Sachdanandam P. Energy-modulating vitamins—a new combinatorial therapy prevents cancer cachexia in rat mammary carcinoma. Br J Nutr. 2005 Jun;93(6):901-9.
28. Folkers K. Relevance of the biosynthesis of coenzyme Q10 and of the four bases of DNA as a rationale for the molecular causes of cancer and a therapy. Biochem Biophys Res Commun. 1996 Jul 16;224(2):358-61.
29. Portakal O, Ozkaya O, Erden IM, et al. Coenzyme Q10 concentrations and antioxidant status in tissues of breast cancer patients. Clin Biochem. 2000 Jun;33(4): 279-84.
30. Ren S, Lien EJ. Natural products and their derivatives as cancer chemopreventive agents. Prog Drug Res. 1997;48:147-71.
31. Palan PR, Mikhail MS, Shaban DW, Romney SL. Plasma concentrations of coenzyme Q10 and tocopherols in cervical intraepithelial neoplasia and cervical cancer. Eur J Cancer Prev. 2003 Aug;12(4):321-6.
32. Jolliet P, Simon N, Barre J, et al. Plasma coenzyme Q10 concentrations in breast cancer: prognosis and therapeutic consequences. Int J Clin Pharmacol Ther. 1998 Sep;36(9):506-9.
33. Gorelick C, Lopez-Jones M, Goldberg GL, Romney SL, Khabele D. Coenzyme Q10 and lipid-related gene induction in HeLa cells. Am J Obstet Gynecol. 2004 May;190(5): 1432-34.
34. Available at: Accessed November 11, 2005.
35. Iarussi D, Auricchio U, Agretto A, et al. Protective effect of coenzyme Q10 on anthracyclines cardiotoxicity: control study in children with acute lymphoblastic leukemia and non-Hodgkin lymphoma. Mol Aspects Med. 1994;15 Suppls207-12.
36. Kawase I, Niitani H, Saijo N, Sasaki H, Morita T. Enhancing effect of coenzyme, Q10 on immunorestoration with Mycobacterium bovis BCG in tumor-bearing mice. Gann. 1978 Aug;69(4):493-7.
37. Folkers K, Wolaniuk A. Research on coenzyme Q10 in clinical medicine and in immunomodulation. Drugs Exp Clin Res. 1985;11(8):539-45.
38. Folkers K, Morita M, McRee J, Jr. The activities of coenzyme Q10 and vitamin B6 for immune responses. Biochem Biophys Res Commun. 1993 May 28;193(1):88-92.
39. Folkers K, Hanioka T, Xia LJ, McRee JT, Jr., Langsjoen P. Coenzyme Q10 increases T4/T8 ratios of lymphocytes in ordinary subjects and relevance to patients having the AIDS related complex. Biochem Biophys Res Commun. 1991 Apr 30;176(2):786-91.
40. Barbieri B, Lund B, Lundstrom B, Scaglione F. Coenzyme Q10 administration increases antibody titer in hepatitis B vaccinated volunteers—a single blind placebo-controlled and randomized clinical study. Biofactors. 1999;9(2-4):351-7.
41. Cortes EP, Gupta M, Chou C, Amin VC, Folkers K. Adriamycin cardiotoxicity: early detection by systolic time interval and possible prevention by coenzyme Q10. Cancer Treat Rep. 1978 Jun;62(6):887-91.
42. Conklin KA. Coenzyme q10 for prevention of anthracycline-induced cardiotoxicity. Integr Cancer Ther. 2005 Jun;4(2):110-30.
43. Samson KJ. Innovative research and applications for CoQ10. Life Extension. August, 2004: 46-55.
44. Lockwood K, Moesgaard S, Yamamoto T, Folkers K. Progress on therapy of breast cancer with vitamin Q10 and the regression of metastases. Biochem Biophys Res Commun. 1995 Jul 6;212(1):172-7
45. Available at: 5. Accessed October 31, 2005.
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These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure or prevent any disease. The information provided on this site is for informational purposes only and is not intended as a substitute for advice from your physician or other health care professional or any information contained on or in any product label or packaging. You should not use the information on this site for diagnosis or treatment of any health problem or for prescription of any medication or other treatment. You should consult with a healthcare professional before starting any diet, exercise or supplementation program, before taking any medication, or if you have or suspect you might have a health problem. You should not stop taking any medication without first consulting your physician.

Water and Frequency Studies

Study the 30 kHz square wave
Study the effects of 30 kHz, square waves, ¼ volt positive offset, on bacteria and parasites in the patient as well as in vitro.
White blood cell reaction to water exposed to specific frequencies
Study the response of white blood cells to drops of water containing the frequency pattern of:
a. An organ
b. Medicine
Drops should be taken under the tongue in repeated doses.
Study the memory of water
Find a way to create, measure and verify existence of square wave frequency in water. Study the change of the frequency. Same with sine wave in water.

Lugol's Lodine

Leading Research Questions
Is Lugol’s effective against food poisoning? What are the pros and cons of using Lugol’s for the purpose of reducing salmonella in stomach?
Working Hypothesis
Taken internally, Lugol’s may help restore immunity caused by iodine-deficiency in the thyroid. In cases of occasional food poisoning or ingestion of contaminated food, Lugol’s may help create a normal internal environment in the stomach that is inhospitable to harmful bacteria that cause gas, bloating, heartburn, indigestion, diarrhea and vomiting.
Lugol’s Iodine was first developed by the French physician, Jean Lugol, in 1829. It was a transparent brown liquid consisting of 10 parts potassium iodine to 5 parts iodine to 85 parts of distilled water. Lugol’s proved an effective bactericide and fungicide and, in fact, was, for the better part of a century, a common antiseptic. Historically speaking, Lugol’s has long been traditionally used to soothe the discomfort of upset stomach due to food poisoning. This use of Lugol’s has thus far not been confirmed by scientific testing.
Traditional Use and Dr. Clark’s Theory
There are many traditional uses of Lugol’s, including taking 6 drops of 4% iodine solution in a ¼ glass of water, then repeating that up to 4 times per day. We have numerous reports that this method stops both diarrhea and throwing up within 3 to 5 minutes of taking the first dose.
Dr. Clark was an avid user of Lugol’s. She claims that it is so effective in killing Salmonella bacteria because the overgrowth of Salmonella is concentrated in the top region of the stomach, near the esophagus. “It floats on top and triggers the body to throw up as it putrefies and expands,” she claimed. Drinking a glass of water containing a prescribed number of drops of Lugol’s will therefore immediately kill much of the Salmonella the moment it enters the stomach.
Overgrowth of Salmonella concentrated in the top region of the stomach, near the esophagus, are easily killed with Lugol’s.
Pros and Cons of using Lugol’s
Many organs in the body require iodine to function normally, especially breast tissue. Recent studies have confirmed an increase in abnormal breast tissue since many commercial bakers eliminated iodine from bread approximately 20 years ago and replaced it with bromine. Excessive bromine is toxic to the thyroid gland as well.
Iodine is necessary for the thyroid gland’s proper performance of its work. The human thyroid gland is located in the front of the lower part of the neck. All the blood in the body passes through the thyroid gland every 17 minutes. Because the cells making up this gland have an affinity for iodine, during this 17-minute passage the gland’s secretion of iodine kills weak microorganisms that may have gained entry into the blood through an injury to the skin, the lining of the nose or throat, or through absorption of food from the digestive tract. Strong, microorganisms are rendered weaker during their passage through the thyroid gland. With each 17 minutes that rolls around they are made still weaker until finally they are killed if the gland has its normal supply of iodine. If it does not, it cannot kill harmful microorganisms circulating in the blood as Nature intended it should.
It is well established that the iodine content of the thyroid gland is dependent upon the iodine available in the food and water intake of the individual. If the iodine intake is low the gland is deprived of an element it needs to do its work.
Safety Evidence of Iodine
Previous deficiency of iodine can cause hypersensitivity. Although toxic effects are not observed in humans until daily intakes have exceeded 10,000 mcg, intakes of 2,000 mcg should be regarded as excessive and potentially harmful (Hetzel and Clugston 1999). Residents of coastal regions in some areas of Japan have chronic daily intakes of iodine as high as 50,000 to 80,000 mcg. Persons who have not been conditioned by iodine deficiency can maintain normal thyroid size and function when they are consuming several milligrams of dietary iodine per day, but previous deficiency can cause hypersensitivity (Hetzel and Clugston 1999). In such situations, hyperthyroidism and iodine-induced thyroiditis may occur when intakes exceed approximately 200 to 300 mcg per day.


Leading Research Questions

1. Study effects of herbal organ cleansing
2. Study free cyanide and the enzyme rodanese in cancer patients
Study effects of Dr. Clark protocols have on cancer
How do blood analysis and other cancer markers change before and after Dr. Clark’s protocols (including dietary changes)
Study A: Herbal organ cleansing studies
· Parasite Cleanse with Colon Cleanse
· Kidney Cleanse
· Liver Cleanse
Study B: Intense cleansing program study
· See schedule of supplements.
· Please find complete protocol in Dr. Clark’s latest book, Prevention and Cure for All Cancers.
Study free cyanide and the enzyme rodanese in cancer patients
Working Hypothesis
Recently, Dr. Clark identified promethium, a lanthanide, as a natural protection from cancer. But when chlorination (bleach) is added to water it introduces cyanide, which displaces promethium, and we end up with low-level chronic cyanide toxicity. Polonium, radium and other radioactive contaminants may adversely affect the DNA replication process, thereby increasing the possibility of mutation. Based on these preliminary findings, Dr. Clark had asked universities to undertake the following:

  1. Measure levels of free cyanide in cancer patients compared to non-cancer patients.
  1. Verify the absence or diminished levels of Cytochrome C3 (food-oxidizing enzyme) in cancer patients.
  1. Quantify levels of the enzyme rodanese in the tumors of cancer patients. The main enzyme that detoxifies cyanide, rodanese, is absent near the tumor in cancer patients, according to Dr. Clark’s findings. A buildup of cyanide occurs, as a result, close to tumors.