CURES for Diabetes

### Cures for DIABETES:

## Dr. J. F. Dice – Stanford University Study-

was able to reduce insulin by 2.5 units for every gram of vitamin C added to his diet.

Dr. Dice gradually increased his vitamin C level – over 23 days – until he reached 11 grams.He took small amounts throughout the day.Taking it with meals is very helpful for absorbing other necessary nutrients.

It is VERY IMPORTANT to test your Blood Sugar Often while you are adding these substances to your diet and reducing your intake of insulin.The biggest danger is “Insulin Shock” – low blood sugar – caused by taking too much insulin.Always carry candy or a high sugar nutritional bar with you if you are diabetic and taking insulin!!!

Also, it is important that you keep a diary noting not only what you are taking when, and your resulting blood sugar level, but additionally make notes regarding your feelings and body reactions.You should always take this diary with you when you go to consult with your doctor.I know far too many people who have gotten into trouble from taking too much insulin.You need to learn how to control your own dose.Here is how insulin works.

Dr. T. C. McDaniel ( ) has managed to help many of his patients to get off of insulin completely at his clinic in Ohio.When you put all the knowledge here together into one program, you have a very Spectacular Cure.

Dr. McDaniel has also saved many diabetic legs from being amputated by restoring circulation with Di-Sodium EDTA Treatments ( ).

Here is an EDTA program you can do at home ( ).

## Nitric Oxide:It’s Role in Diabetes, Peripheral Neuropathy, and Wound Healing

The Nobel Prize was awarded to three Americans in 1998 for their work on discovering NO (Nitric Oxide) and clarifying its role in health.Their most important contributions lay in describing the effect of NO on the circulation that, as everyone knows, is disturbed to one degree or another in diabetic patients.

The question then becomes is NO metabolism or action deranged in diabetic patients and could NO have a role in preventing some of the consequences in diabetes?

Dr. Tom Burke received his PhD in Physiology from University of Houston, Post Doctoral Training at Duke Medical School, He was an Associate Professor of Medicine and Physiology at the University of Colorado Medical School. He has authored more than 70 published scientific clinical articles and has been a visiting scientist at the Mayo Clinic, Yale University, University of Alabama, and University of Florida. He is a recognized international lecturer on cell injury and nephrology.

## Meningococcal Vaccine is a “Potential Time Bomb”

A study published in 2002 in the medical journal “Autoimmunity” showed that the Meningococcal Vaccine was responsible for a 26% increase in diabetes in the 100,000 children who received the vaccine as part of a clinical trial.

Significantly, it was not until 3-4 years after the vaccine was administered that most of the vaccine-related cases of diabetes were diagnosed.

It is of great concern to me also that the MeNZB vaccine contains Aluminum Hydroxide ( ), which was identified as being carcinogenic in animal tests as far back as 1975.

Cancer already kills more New Zealand children than any other disease. I don’t believe that it makes good sense to inject babies, children or teenagers with a known carcinogen when cancer is already such a serious public health problem in this country, for adults and children alike.”

What Your Doctor Will Never Tell You, By Katherine Joyce Smith, PDF file at: vaccine issue.pdf

– Also See… Vaccination Hazards

MSG Triples the Amount of Insulin the Pancreas Creates

## Hemochromatosis, iron overload could cause diabete:

Hemochromatosis is often undiagnosed and untreated. It is considered rare and doctors may not think to test for it. The initial symptoms can be diverse and vague and can mimic the symptoms of many other diseases. Also, doctors may focus on the conditions caused by hemochromatosis-arthritis, liver disease, heart disease, or diabetes-rather than on the underlying iron overload. However, if the iron overload caused by hemochromatosis is diagnosed and treated before organ damage has occurred, a person can live a normal, healthy life.

If the disease is not detected early and treated, iron may accumulate in body tissues and may eventually lead to a serious problem such as damage to the pancreas, possibly causing diabetes.

Doctors should consider testing people who have joint disease, severe and continuing fatigue, heart disease, elevated liver enzymes, impotence, and diabetes, because these conditions may result from hemochromatosis.

The National Digestive Diseases Information Clearinghouse (NDDIC) is a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The NIDDK is part of the National Institutes of Health under the U.S. Department of Health and Human Services. Established in 1980, the Clearinghouse provides information about digestive diseases to people with digestive disorders and to their families, health care professionals, and the public. The NDDIC answers inquiries, develops and distributes publications, and works closely with professional and patient organizations and Government agencies to coordinate resources about digestive diseases.

National Digestive Diseases Information Clearinghouse, 2 Information Way, Bethesda, MD 20892-3570

## Dietary Chromium: An Overview, By Barry Mennen, M.D., Executive Director, Chromium Information Bureau, Inc.

Discovery of Chromium’s Role in Human Health

It was known by the 1950s that chromium was required by animals to control blood sugar, but it wasn’t until the 1970s that chromium’s essential role in humans was clearly proven. This proof came accidentally, as a result of a new procedure that had been introduced to nourish hospitalized patients who could not take in any food by mouth. This procedure, giving specially made feeding solutions directly through the patient’s vein, is referred to as Total Parenteral Nutrition or TPN.

TPN was designed to give patients all the carbohydrates, proteins, fats, vitamins and minerals they needed to maintain health until they could once again eat normally and obtain these nutrients from food. Some of these patients who had been fed intravenously for months developed high blood sugars just as if they were diabetic (which they weren’t). The doctors then had to start insulin therapy in order to treat this diabetes-like condition and even then the insulin they were given didn’t appear to work as well as it should have.

Since it was already known that chromium was necessary for insulin action, it was thought that this trace element may have been lacking in these patients’ TPN solutions. Thus it was deduced that these patients were showing signs of very severe chromium deficiency. The physicians caring for them then added chromium in very small amounts less than 50 micrograms (abbreviated as mcg; equal to 1/1000 of a milligram) to their IV feeding solution and quickly noted an improvement.

Chromium and Diabetes

Because of chromium’s connection to insulin function, it should come as no surprise that most of the research with this trace mineral relates to diabetes or to non-diabetic persons who develop high blood glucose levels after ingesting simple sugar. There are at least 16 clinical studies, which have tested specific chromium compounds in such patients using proper scientific methods (other studies on chromium supplementation in diabetics which used questionable methods in their study design are not included in the following summary).

While three of the 17 properly designed studies showed no benefit of chromium supplementation in diabetics, 14 did show blood glucose improvements in the patients tested. For example, a recent study that has been reported (which was presented in 1995 at the annual meeting of the American College of Nutrition) showed dramatic improvements in blood sugar using less than one milligram of supplemental chromium picolinate in a group of women who developed gestational diabetes (that is, they showed symptoms and signs of diabetes only during their pregnancies).

The latest study to examine the issue of chromium supplementation and adult-onset diabetes was presented in June, 1996 at the annual Scientific Sessions of the American Diabetes Association held in San Francisco, CA. Researchers from the Human Nutrition Research Center of the United States Department of Agriculture collaborated with Chinese researchers from the Beijing Medical University.
They randomized 180 adult-onset diabetics into 3 groups of 60 each: one group received placebo twice per day, the second received 100 mcg twice daily of chromium as chromium picolinate and the third received 500 mcg of chromium as chromium picolinate twice daily. Their blood work was examined at baseline, at 2 months and at 4 months.
The patients were told to remain on their anti-diabetic medications and continue with their diets and activity levels as before.

The results were impressive: blood glucose, insulin levels, cholesterol and glycated hemoglobin (a measure of blood sugar control over the previous few months) all decreased, with the higher dose generally (but not always) more effective than the 200 mcg.

How could such tiny amounts of chromium have such profound effects on insulin’s action? Again, the answer is not known with certainty, but the evidence so far suggests that chromium strengthens certain effects of insulin on the body’s cells; in other words, it doesn’t work by stimulating the body to make more insulin, but rather chromium makes the insulin, which is present function more effectively in the cells of the body.

When the body does not respond to insulin in the normal manner, doctors refer to this as insulin resistance. Insulin resistance signifies that the insulin, which is circulating in the blood, is not able to have its usual effects on various tissues in the body. This is not the problem with the type of diabetes (referred to as type I or juvenile-onset) that strikes young children: these individuals cannot make insulin anymore and thus must take it by injection. However, most diabetics suffer from maturity-onset diabetes (or type II; increasingly referred to as NIDDM or non-insulin dependent diabetes mellitus; this type of diabetes affects 90% of people with the disease).

It is these patients with NIDDM who demonstrate insulin resistance and are the ones most at risk for chromium deficiency and its consequences. Further, there is some evidence that marginal chromium deficiency may be important in other areas of health and disease. These other diseases where chromium may be important are some of the most common and significant illnesses of industrialized nations (see below).

The following is the ending to the chapter on chromium nutrition in the latest edition of the standard reference textbook on medical nutrition:

“Based on current knowledge of chromium function and nutrition, the possibility cannot be ignored that inadequate chromium status may be responsible in part for some cases of impaired glucose tolerance, ‘hyperglycemia, hypoglycemia. glycosuria [sugar in urine], and refractoriness to insulin.”

Modern Nutrition in Health and Disease, Eighth Ed.., 1994. Shils, Olson and Shike, eds.

HEALTH NOTEIt is important to note that persons with diabetes who are on insulin or other anti-diabetic medications should check with their doctors before supplementing their diets. Because chromium may decrease the amount of insulin resistance present, it may change the type or amount of medication needed to treat the diabetes and/or the frequency with which blood sugar monitoring needs to be done.
This is especially important for those persons with diabetes who are under tight blood glucose control. Adding supplemental chromium in this situation has the potential to cause low blood sugar (hypoglycemia).

The Insulin Resistance Syndrome (Syndrome X; Reaven’s Syndrome; Insulin-Metabolic Syndrome)

The combination of obesity, diabetes, hypertension (high blood pressure) along with abnormalities in blood cholesterol and fat (lipid) has long been noted in the medical literature. By the late 1980s, a noted diabetes expert from Stanford University (Dr. Gerald Reaven) proposed that the basic combination of high blood sugar, high blood pressure and abnormal blood lipids all constituted disease that was based on increased insulin resistance; he noted that while increased insulin resistance is the first step in the development of maturity-onset or type II diabetes, it is the body’s response to the insulin resistance which determines whether or not the individual becomes a diabetic or not.

“Even if high blood sugar does not develop, insulin resistance does not appear to be a good thing to have: The fact that an insulin-resistant subject may not become diabetic does not mean that they suffer no untoward consequences. Indeed, an argument can be made that the more insulin sensitive an individual, the better off he or she is, and that the attempt to compensate for insulin resistance sets in motion a series of events that play an important role in the development of both hypertension and coronary artery disease.

Reaven GM. Role of Insulin Resistance in Human Disease. Diabetes, 37:1595, Dec., 1988.

Since chromium reduces insulin resistance, this essential trace element could therefore have wide-ranging effects on high blood pressure and abnormal blood lipids in addition to lowering blood sugar.

However, Dr. Reaven did not connect any insulin resistance to possible marginal chromium status, and we cite him here only to point out his contribution to describing this syndrome. It is also important to note that while studies in peer-reviewed medical journals have shown that chromium supplementation lowers blood lipids such as triglycerides, for now there are no human data on chromium and blood pressure.


Indications are that marginal deficiency of chromium, an essential trace mineral, may be widespread in industrialized nations. Further, the consequences of this deficiency may contribute to some of the manifestations of obesity, diabetes, abnormal blood lipids, hypertension and coronary artery disease in 20th century western society.

Although some of the above is speculative, it would seem prudent for Americans to supplement their diets with small amounts of trivalent chromium (for example, 200 mcg of chromium picolinate) since the benefits of supplementation may be significant for certain individuals and the safety of this regimen is well-supported by a large amount of data.


It is extremely difficult to poison laboratory animals with oral chromium. For example, cats fed 1,000 mg of trivalent chromium per day showed no signs of toxicity (the equivalent daily dose for a 150 lb person would be approximately 35,000 mg per day or 3.5 million mcg per day. In terms of the number of 200 mcg tablets, this would be 175,000 tablets per day for a human.

On March 14, 1996, a safety study conducted by the U. S. Department of Agriculture was presented at the Society of Toxicology’s annual meeting. This study looked at various supplemental doses (including none) of chromium chloride and chromium picolinate fed to rats for 6 months, The highest doses were equal to a human consuming 5,000 tablets of 200 micrograms chromium picolinate. At regular intervals during the study the rats were weighed and blood was taken for laboratory tests.
At the end of the study the livers and kidneys (organs that would have the highest tissue levels of chromium) were examined under the microscope. There were no differences in any of the measurements or examinations between the various groups. The investigators were unaware (“blinded”) as to which group the animals were in when the measurements and evaluations were performed.

The Chromium Information Bureau, Inc. March, 1966; revised November, 1996. Permission is granted to reproduce this information.


## Eliminate man-made/processed fats, such as trans and hydrogenated fats, and supplement Omega-3 rich oils.

“Research has shown that an Omega-3 Index of 8 percent to 10 percent reduces a person’s relative risk of death from coronary heart disease by 40 percent, and from sudden cardiac death by 90 percent.

” This benefit probably results from restored insulin-mediated glucose/vitamin C uptake into cells.

[See: Protocol for Reversing Diabetes Type II by Eliminating Hydrogenated and Trans Fats and adding Omega-3 oils… ] : ,a href=”” target=_blank>

Note: Following an Atkins-style diet will eliminate most trans fats because these “poisons” appear mostly in processed carbohydrate foods such as cookies, crackers, snacks, etc. Butter is vastly supperior to margarine. Natural saturated fats are vastly superior to any fats or oils processed for longer shelf life.

## The Cure for Non-Insulin-Dependent (Type II) Diabetes.

Reversing Diabetes Type II, Glucose-Ascorbate Antagonism, and their Impact on Reversing Heart Disease (2005)

## Dr. RATH Therapy successes in curing diabetes or

For my patients with diabetes, especially non-insulin dependent patients, I have seen very rapid response rates, usually within the first few weeks of treatment. In those patients, I have been able to gradually reduce their medications as well. In at least ten cases, patients that would have otherwise required amputation have been able to avoid that procedure by implementing Dr. Rath’s nutrient synergy recommendations.

Diabetes’ Testimonials

# Richard Polk – Condition: Diabetes

I was diagnosed with diabetes six years ago. I didn’t have the energy that I had before I started taking [cellular nutrients]. After I started taking them, I got more energy. I feel much better. I can move around much better. I can run. I can walk distances. I can walk a mile!

# Mary Bivins – Condition: Diabetes

My name is Mary Bivins and I am 46 years old. Before I started taking cellular nutrients, I couldn’t walk one flight of stairs. I couldn’t do laundry that much, because I had to go downstairs to wash. But about two weeks after I started taking, I could do all of that. I couldn’t even walk to the store without getting tired. My fiancé was always telling me, “You don’t walk with me.” But now, every time he gets ready to go, I’m right there with him. I walk with him, and my mother sees I can walk up and down the stairs without getting tired. She asked me what was I doing to do this and to get my energy back. [Cellular nutrients] help me a lot and I will continue to take them because they really help me. When I first learned I had diabetes, I worked for a while and then I had to come off. I was having problems with my knees and my legs, but now everything seems to be better.

## Biotin has been found to benefit Diabetes

Biotin Deficiency– Eczema, improper fat metabolism, RDA- 300 mcg, Optimal intake- 300-10,000 mcg

Good Sources- Brewer’s yeast, soy beans, egg yolk

Discussion- A Biotin deficiency is rare. Unless raw egg whites are eaten often (they contain a substance that binds Biotin), we get ample Biotin. Recently high-dose Biotin has been found to benefit Diabetes.

Also known as Coenzyme R, Factor W, Factor S, Factor H, Factor X, and Vitamin H

Vitamin N*, Chemical Names- Thioctic Acid, Alpha-lipoic acid. Deficiency- lack of growth in protozoa and bacteria. Optimal intake- 300-600 mg. Discussion- A-Lipoic Acid has been used recently in Diabetes treatment.

## Prolonged deterioration of endothelial dysfunction in response to postprandial lipaemia is attenuated by vitamin C in Type 2 diabetes.

Diabet Med. 2006 Mar;23(3):258-64.
Wales Heart Research Institute, University of Wales, College of Medicine, Cadddif, Wales.

BACKGROUND: Endothelial dysfunction (ED) has been described in Type 2 diabetes (T2DM). We have described previously a diminution of flow-mediated arterial dilatation and, by implication, further ED in T2DM in response to postprandial lipaemia (PPL) at 4 h. This is possibly mediated by oxidative stress/alteration of the nitric oxide (NO) pathway. T2DM subjects tend to exhibit both exaggerated and prolonged PPL. We therefore studied the relationship of PPL to the duration of ED in T2DM subjects and oxidative stress with or without the antioxidant, vitamin C.

METHODS: Twenty subjects with T2DM with moderate glycaemic control (mean HbA1c 8.4%) were studied. After an overnight fast, all subjects consumed a standard fat meal. Endothelial function (EF), lipid profiles, and venous free radicals were measured in the fasting, peak lipaemic phase (4 h) and postprandially to 8 h. The study was repeated in a double-blinded manner with placebo, vitamin C (1 g) therapy for 2 days prior to re-testing and with the fat meal. Oxidative stress was assessed by lipid-derived free radicals in plasma, ex vivo by electron paramagnetic resonance spectroscopy (EPR) and by markers of lipid peroxidation (TBARS). Endothelial function was assessed by flow-mediated vasodilatation (FMD) of the brachial artery.

RESULTS: There was a significant decrease in endothelial function in response to PPL from baseline (B) 1.3 +/- 1.3% to 4 h 0.22 +/- 1.1% (P attenuated at each time point with vitamin C. Baseline EF with vitamin C changed from (fasting) 3.8 +/- 0.9-2.8 +/- 0.8 (at 4 h) and 2.9 +/- 1.3 (at 8 h) in response to PPL. Vitamin C attenuated postprandial (PP) oxidative stress significantly only at the 4-h time point [301.1 +/- 118 (B) to 224.7 +/- 72 P
CONCLUSION: PPL is associated with prolonged endothelial dysfunction for at least 8 h after a fatty meal. Vitamin C treatment improves endothelial dysfunction at all time points and attenuates PPL-induced oxidative stress. This highlights the importance of low-fat meals in T2DM and suggests a role for vitamin C therapy to improve endothelial function during meal ingestion.

PMID: 16492208 [PubMed – in process]

## Vitamin E may help some diabetics

Main Category: Cardiovascular/Cardiology News ( ), Article Date: 20 Nov 2004 – 0:00am (UK)

Despite recent reports that show use of high-dose vitamin E supplements is associated with a higher overall risk of dying, at least one group stands to benefit greatly from the same vitamin. About 40 percent of diabetic patients can reduce their risk of heart attacks and of dying from heart disease by taking vitamin E supplements, according to a Technion-Israel Institute of Technology study published in the November 2004 Diabetes Care ( ).

The research team, led by Dr. Andrew Levy of the Faculty of Medicine, had earlier demonstrated that diabetics with a particular form of a blood protein called haptoglobin had as much as a 500% increased risk of developing heart disease. The new study shows that when these at-risk patients, who have the 2-2 form of haptoglobin, took 400 international units of vitamin E daily, they reduced their risk of heart attack by 43 percent ( ), and their risk of dying of heart disease by 55 percent.

About 40% of diabetics have the 2-2 form of haptoglobin; the rest have the 1 -1 or 2-1 forms. When they took the same vitamin E supplements, they did not show any significant reduction of cardiovascular risk resulting from vitamin E therapy.

Dr. Levy’s study analyzed serum samples that had been stored from the Heart Outcomes Prevention Evaluation (HOPE) trial of 2000, designed to study the effect of antioxidant therapy such as vitamin E on cardiovascular risk. The results of that study showed no benefit from vitamin E therapy on cardiovascular risk. However, Dr. Levy notes, the study did not segregate patients according to their haptoglobin type, analyzing instead the benefits of vitamin E in all patients. When he studied the serum samples from the HOPE study according to haptoglobin type, he found the greatly reduced risks noted above.

Now, a large-scale, five-year study of some 2,000 diabetics with haptoglobin 2-2, being conducted in northern Israel, is expected to corroborate Dr. Levy’s findings.

“If this larger study confirms our findings, the public health implications will be huge. Vitamin E would represent an inexpensive and safe way to reduce the risk of cardiovascular death and heart attack in a significant proportion of diabetic patients,” he said.

Dr. Levy had demonstrated in multiple previous studies that haptoglobin 2-2 is predictive of heart disease — but only in people with diabetes. That’s because diabetics tend to have more free radicals that destroy antioxidants. Furthermore, haptoglobin 2-2 is a very poor antioxidant when compared to the other haptoglobin types. This combination means that diabetics with haptoglobin 2-2 have an even greater deficiency of antioxidants than do diabetics with the other haptoglobin variants. Therefore, an increased supply of antioxidants, such as those found in vitamin E, would be expected to provide the greatest benefit for these patients.

The Technion-Israel Institute of Technology and the Kennedy-Leigh Charitable Trust is funding the new study. Dr. Levy is partial owner of a patent for a blood test that predicts susceptibility to diabetic vascular disease based on haptoglobin type.

The Technion-Israel Institute of Technology is Israel’s leading science and technology university. Home to the country’s only winners of the Nobel Prize in science, it commands a worldwide reputation for its pioneering work in computer science, biotechnology, water-resource management, materials engineering, aerospace and medicine. The majority of the founders and managers of Israel’s high-tech companies are alumni. Based in New York City, the American Technion Society is the leading American organization supporting higher education in Israel, with more than 20,000 supporters and 17 offices around the country.

Contact: Kevin Hattori,, 212-407-6319

## Need for Vitamin E

Many factors affect vitamin E levels in the human body. Thyroid hormones, cholesterol-lowering drugs and consumption of unsaturated fats reduce blood serum levels of tocopherols.

Another problem in assessing the need for vitamin E is its relationship with cholesterol. Vitamin E is carried from the liver to tissues on cholesterol particles. There is an over-reliance upon measurements of blood serum vitamin E levels rather than tissue levels. In 1972, MK Horwitt and colleagues noted that the blood carries only about 1 percent of the tocopherols in the body. Furthermore, as cholesterol levels drop in the blood circulation, so do circulating levels of the tocopherols. It’s no coincidence that as total cholesterol drops below 160 mg per deciliter that the risk of cancer more than doubles. There is simply less vitamin E reaching tissues as cholesterol concentrations decline.

Even though there is evidence that dietary and supplemental vitamin E is helpful in reducing the risk of cataracts and certain forms of cancer and vitamin E is beneficial for diabetes, the primary focus for this vitamin has been in reducing cholesterol and the overall risk of heart disease.

In the 1960s the Shute brothers of London, Ontario, Canada utilized mega-dose vitamin E to remedy cases of angina and heart disease with reported success. But this only proves that vitamin E is helpful for people with heart and blood vessel disease. Again, what about healthy individuals?

Since vitamin E travels on cholesterol particles produced in the liver for transport to tissues, it also protects circulating blood fats from oxidizing and hardening in blood vessel walls. So vitamin E should produce cardiovascular health benefits.

## from THE HEALING FACTOR / VITAMIN CAgainst Diabetes, by Irvin Stone,



By Irwin Stone, With forewords by Nobel PrizewinnersDr. Linus Pauling and Dr. Albert Szent-Gyorgyi

Vitamin C may save your life!A noted biochemist reveals for laymen the exciting research into ascorbic acid’s powers against such deadly enemies as cancer, heart disease, strokes, mental illness, old age, diabetes, arthritis, kidney disease, hepatitis — even cigarette smoking!

Sir Archibald, in his original 1908 papers, described four genetic diseases but the list has now grown and new ones are constantly being reported.He reported on albinism, alkaptonuria, cystinuria and pentosuria, all due to the lack of a particular enzyme in the afflicted individual’s biochemical inheritance.Albinism, a relatively harmless condition, is due to the lack of an enzyme used in the production of the black skin pigment, melanin.Alkaptonuria and cystinuria are both diseases of protein metabolism in which the missing enzyme causes an accumulation of intermediate protein digention products, which causes changes in the urine and other parts of the body.Alkaptonuria is relatively benign until late in life when it produces a severe type of arthritic condition.Cystinuria induces the formation of kidney and bladder stones, while the relatively rare and harmless pentosuria causes pentose, a sugar, to appear in the urine and may be confused with diabetes.

Like many other great discoveries in medicine, Garrod’s work was almost ignored for a generation.In fact, an examination of the major genetics textbooks in use in 1940 fails to reveal any mention of alkaptonuria, described by Garrod thirty-two years earlier.Time has corrected this oversight and the importance of Garrod’s pioneering work is now acknowledged by all.


Diabetes and its opposite counterpart, hypoglycemia, are diseases caused by disturbances in the delicate balance of the sugar chemistry of the body.The sugar, glucose, is a normal blood constituent and is used by the body as a source of energy.To utilize this energy the body requires insulin and some 20 enzymatic chemical reactions.

For the normal functioning of the human body, the concentration of glucose in the blood must be maintained within narrow limits (the normal range is 80 to 120 mg).The biochemical traffic policeman that controls the level of glucose in the blood is insulin.Insulin is produced in a part of the pancreas called the Islets of Langerhands, from where it enters the bloodstream.

Since the amount of glucose in the blood may vary, such as after eating, the insulin must be doled out by the pancreas in just the right amounts.Too little insulin circulating in the blood permits the glucose levels to rise (hyperglycemia) and brings on the diabetic state.When the blood level of glucose rises above the height of the kidney dam of 170 mg % (kidney threshold) it spills over into the urine and positive urinary sugar tests result.Too much insulin in the blood is equally bad because it produces the condition of hypoglycemia (low blood sugar) and there are probably as many people suffering from this serious condition as from diabetes.

In the treatment of diabetes, insulin is injected because, if given orally, it is destroyed by the digestive enzymes.The dosage of insulin requires careful control because if it is too much, low bloodsugar, or “insulin shock,” will result.A test used to determine whether pancreatic secretion of insulin is normal or not is the so-called glucose-tolerance test.A large amount of glucose sugar is fed the fasting patient.The blood glucose values are determined before and at hourly intervals after ingesting the sugar.From the result obtained it is possible to distinguish normality, diabetes (too little insulin), and hypoglycemia (too much insulin).If the body has an excess of sugar beyond its immediate needs, it is converted to the insoluble carbohydrate, glycogen, which is deposited in the liver for storage.Thus a sugar reserve is available and, in times of need, glycogen can be converted back into the soluble sugar, glucose.

An estimated 4 million Americans have diabetes and about 1/2 of these are undiagnosed.Heredity is important because, in about 50 percent of the cases, there is a familial history of diabetes.It has also been estimated that about 22 percent of the United States population carries the recessive gene for this disease.Diabetes ranks eighth as a cause of death in the United States and it is the third leading cause of blindness.The importance of maintaining the delicate biochemical balance of insulin, therefore, cannot be underrated.The use of insulin for the treatment of diabetes began in the 1920s and the Canadians, Frederick Banting and John Macleod, received the 1923 Nobel Prize in Biochemistry for its discovery.

Not long after the discovery of ascorbic acid in the early 1930s, tests on guinea pigs indicated that ascorbic acid had a profound influence on the body’s sugar utilization.In 1934, C.G. King and coworkers (1), at the University of Pittsburgh, showed that guinea pigs maintained on low levels of ascorbic acid developed degeneration of the Islets of Langerhands.Guinea pigs depleted of ascorbic acid showed a low glucose tolerance which was rapidly regained on feeding them ascorbic acid.In 1935 and 1937, they also demonstrated that injection of sublethal doses of diphtheria toxin (increased stress) further diminished their tolerance to sugar in proportion to the length of their ascorbic acid deprivation.

These results were confirmed and extended in a comprehensive series of papers from India by Banerjee (2), starting in 1943.He not only confirmed that guinea pigs with scurvy showed poor sugar tolerance, but indicated that the insulin content of the pancreas of scorbutic guinea pigs is reduced to about 1/8 that of normal guinea pigs.He observed grosschanges in the microscopic appearance of sections of the pancreas from scorbutic guinea pigs. The appearance returned to normal when the guinea pigs were given ascorbic acid.He also reported that the normal conversion of excess sugar into glycogen reserves for liver storage is also impaired in scurvy.In 1947, using improved laboratory techniques, he confirmed his earlier results and revised his estimate of the insulin content of the pancreas of scorbutic guinea pigs to one-quarter that of normal.He also states in this paper:

The disturbed carbohydrate metabolism as seen in scurvy is due to a deficiency of insulin secretion and a chronic deficiency of this vitamin may be one of the etiological factors (causes) of diabetes mellitus in human subjects.

In 1958, he published the results of additional studies which confirmed his earlier work.His 1964 paper contained the very suggestive results of the work on the intestinal transport of glucose.It was found that the intestinal absorption of sugar was about doubled when the animals were deprived of ascorbic acid and returned to normal when they received ascorbic acid.If this observation is applicable to humans, it would mean that the intestines of diabetics,who may exist on chronic, low levels of ascorbic acid, would permit much more rapid absorption of sugar after eating.The blood sugar levels would rise to higher levels faster and put abnormal stress on the already strained insulin production in their pancreas.

Other workers have reached similar results.In fact, there have been so many papers published that a complete review is impossible in a singlechapter.We will only discuss some very suggestive results on which further research should be expended.Altenburger, in 1936, showed that guinea pigs deprived of ascorbic acid were unable to convert glucose to glycogen for storage in their livers, but this condition was promptly relieved when ascorbic acid was administered.

A dose of insulin that produced a pronounced decline in blood sugar in normal monkeys had little effect on monkeys deprived of ascorbic acid (Stewart and coworkers, 1952).The intimate relationship between insulin and ascorbic acid has been noted numerous times.When insulin is injected, there is a fall in the ascorbic acid levels in the blood serum of man, dogs, and rats, as shown by Ralli and Sherry in 1940 and 1948.Haid, in 1941, also noted this drop, not only after insulin injection but in patients in insulin shock.Previously,in 1939, Wille reported that ascorbic acid is helpful to schizophrenics receiving insulin shock treatments.She also produced evidence that ascorbic acid acts to raise the blood sugar levels in hypoglycemic attacks and said that prolonged administration of ascorbic acid will prevent these low blood sugar attache(3).

Ascorbic acid potentiates the action of insulin and, therefore makes it possible to derive the same effect with much less insulin.This was observed in 1939 by Bartelheimer and was accidently confirmed by Rogoff and coworkers in 1944. (4).Rogoff and his coworkers noted greater sensitivity in two diabetic children to their usual dose of insulin in the diabetic ward of their Pittsburgh hospital.On checking, they found that the children had also been given ascorbic acid and they believed this fact was responsible for the excessive insulin effect.In reviewing the literature, they cite a paper by Dienst, Diemer, and Scheer which reported that the ascorbic acid used in their tests on diabetics was equivalent to the effect of twenty units of insulin.They also mention the work of Pfleger and Scholl (40) who, in 1937, noted that ascorbic acid so improved the action of insulin that a diabetic could control his sugar tolerance with a lower level of insulin.

Such conclusions should have initiated large-scale intensive research to determine how much ascorbic acid is needed to minimize the disagreeable insulin injections and still maintain controlled sugar metabolism and, incidentally, save diabetics millions of dollars.The combination of ascorbic acid with the oral medications may also be helpful in avoiding some of the undesirable vascular side effects of diabetic treatment(5).

Tests were started in the early 1930s to determine if the administration of ascorbic acid would reduce the blood sugar levels of diabetics and this resulted in a large volume of medical literature.As in the treatment of other diseases, with the short-term use of ascorbic acid, the more papers that appeared, the more confusion resulted.Some clinicians reported good results in controlling diabetes and others stated that there was no effect.The pros and cons are too numerous to be reviewed here.It was pointed out, in 1935,that the does used may have been insufficient (6).Whether or not this was true is unimportant; the entire approach to this research work may have been misdirected.The tests were aimed at the short-term application of ascorbic acid to see whether diabetes, caused by an already damaged pancreas, could be controlled. A better approach would have been in the area of prevention:the long-term administration of ascorbic acid to prevent pancreatic damage and the subsequent occurrence of diabetes.Such a plan is explained in the following paragraphs.

There is an assemblage of facts, scattered in the medical literature like pieced of a jigsaw puzzle, which have lain dormant for decades.But when put together, they form the picture for research to possibly prevent the millions of cases of diabetes which develop later in life, especially in individuals who carry the recessive gene for this trait.The pattern of the projected research would be to correct one genetic disease, hypoascorbemia, in order to help prevent the other, diabetes.Here are the facts

Figure 6 not available

Similarity of Molecular Structure of Alloxan and Dehydroascorbic Acid, Especially to Right of Dashed Center Line

1. There is a substance called alloxan which, when injected into laboratory animals, produces diabetes.This has long been known and was used as far back as 1943 as a convenient and rapid means for inducing diabetes in laboratory animals for testing purposes.

2. When ascorbic acid is oxidized, it forms dehydroascorbic acid, a compound similar in structure to alloxan.The structures of ascorbic acid, dehydroascorbic acid and alloxan are shown in Figure 6.One doesn’t have to be a chemist to see the similarity between dehydroascorbic acid and alloxan structures to the right of the midline drawn through the molecule and the dissimilarity of ascorbic acid.The chemical properties of alloxan and dehydroascorbic acid are also strikingly similar, as noted by Patterson in 1950.

3. Like alloxan, the injection of dehydroascorbic acid into rats produces diabetes as was shown by Patterson in 1949 and also produces diabetic cataracts as he showed in 1951.That injection of ascorbic acid does not produce diabetes was shown by Levey and Suter in 1946.

4. Banerjee reported in 1952 that he found no dehydroascorbic acid in the tissues, including the pancreas, of normal guinea pigs but stated, “It was present in considerable amounts in the tissues of scorbutic guinea pigs: (7).

5. The mammalian genetic disease, hypoascorbemia, prevents us from making the mammalian liver metabolite, ascorbic acid.The full correction of this genetic disease provides the rationale for the intake of much higher levels of ascorbic acid (8).

The genetically potential diabetics are those who may develop the diabetic state later in life.During their early years, they have an apparent normal production and secretion of insulin from their pancreas.As a group, they are likely to be more sensitive to factors which may affect the delicate physiological balance which controls insulin production.This is indeed a delicate equilibrium.With too little insulin, diabetes is the result; too much insulin produces the equally serious disease, hypoglycemia.These genetically sensitive individuals have probably existed all of their lifetime on suboptimal levels of ascorbic acid.Even the best diet could not supply their individual requirements.

Finally, chronic ascorbic acid deprivation and depletion pushes them over the brink into a state of abnormal insulin production.This chronic exposure of their pancreas to the consequent high ratios of dehydroascorbic acid may slowly damage the secretory cells beyond the point where normal function or regeneration is possible, and the abnormal sugar responses result.

Diabetes may be prevented by the long-term ingestion of daily optimal amounts of ascorbic acid to keep dyhydroascorbic acid-ascorbic acid ratios at a minimum.The long-term research needed to prove or disprove this thesis will be expensive, but preventing diabetes or hypoglycemia in millions of cases would certainly be worth all the costs.

## Dr. Nieper’s Cure for Diabetes,

” Dr. Nieper’s Revolution in Technology, Medicine and Society “, ISBN 3-925188-07-X
© M.I.T. Management Interessengemeinschaft für Tachyonen-Feld-Energie GmbH
Friedrich-Rüder-Straße 1, 2900 Oldenburg, Federal Republic of Germany, English – May 1985

***Optimizing Our Body’s Immune System to Fight Disease***

By learning about Diseases, we gain a better understanding of How To Stay Healthy.

Leading causes of death in 1997 and the number of “Americans” who died from each. The data are based on an annual review of death certificates by the National Center for Health Statistics.
(Laws have recently been passed forbidding the listing of the cause of death, on death certificates! – [ Out of sight, out of mind? ])

1. Heart disease,725,790 – 83 people per hour. ( )
2. Cancer,537,390 – 61 people per hour. ( )
3. Stroke,159,877 – 18 people per hour. ( )
4. Lung disease,110,637.
5. Accidents**,92,191.
6. Pneumonia and Influenza,88,383. ( )
7. Diabetes,62,332. ( )
8. Suicide,29,725. ( )
9. Kidney disease,25,570. ( )
10. Liver disease,24,765. ( )
11. Blood poisoning,22,604. ( )
12. Alzheimer’s disease,22,527. ( )
13. Homicide,18,774. ( )
14. HIV and AIDS,16,685. ( )
15. Hardening of arteries,15,884 – 2 people per hour.( )

EXAMPLE: Diabetes Mellitus (diabetes)

The orthodox way of treating this disease, which, according to Cheraskin, is the cause of many problems, is to normalize the blood sugar level by ingestion of certain medications that lower the sugar level, or by injection of insulin. In addition, an appropriate diet is prescribed. Rolled oat flakes are particularly favorable. As a rule, this exhausts what orthodox medicine has to offer diabetics. And yet, diabetic patients require larger quantities of zinc for several reasons ( ). They require magnesium carrier compounds and selenium, because the larger and especially the smaller arterial blood vessels can be severely damaged by diabetes, even if a “normal” glucose level is maintained. Furthermore, the patient requires a substance, which is called GTF (glucose tolerance factor) by the California biochemist, Schrauzer, because, similarly to oats, it normalizes the glucose level due to more thorough sugar burning, and because it is necessary to prevent, the damage mentioned to blood vessels and nerves. GTF is a chromium compound.

Zinc aspartate and zinc orotate also stabilize the blood glucose level and reduce the need for insulin. In addition, these substances are effective against the diabetic’s impotence. Orthodox medicine however, rarely, if at all, offers the products mentioned. The same is true for fresh food high in fiber, Selenium-yeast, and diluted hydrochloric acid, which is a source of hydrogen and chlorine ions.

Diabetes is a prevalent cause of severe damage to the retina of the eye often resulting in blindness. For this reason it must be attempted to protect (guard) the arteries of the retina from damage and above all to “seal” them. This can be done with the so-called colamime phosphate salts such as Phosetamine and calcium-EAP. These substances, likewise, may seal the pancreatic islet cells against immune aggression. Furthermore one can improve the “burning” of glucose using medication, which also lowers the level of cholesterol. Bezofibrate is to be mentioned here, however, the eumetabolic Carnitine is substantially better suited for this task. It need not be mentioned that orthodox medicine almost never offers this treatment.

Recently, also, certain activated camphor compounds, , have appeared during research, which are potentially gene-repairing substances. Thus, possibly even the genetic instability “diabetes” may be sealed up by these compounds.

## Pauling’s Therapy and Towers Heart Formula to cure Diabetes

Shortly after that, in January 2001, I was diagnosed with Diabetes Type 2. I was placed on Amaryl and Actos to help lower my sugar, which was 325 pts.

I waited a few months to make sure the Towers Heart Formula was working for me. I then decided to spread the good news. It’s working.

As of this present time, September 1, 2001, I am free of chest pains. My cholesterol is 245. My triglyceriets 176. My LP(a) 10. My sugar ranges between 99 – 130. I take no medicine for Diabetes. I take no Heart medicine, no zorcor, tricor, toprol, micardis, microzide, amaryl and actos. My blood pressure is down from 170/95 to 142/82 . I’m still mending and improving every day with GOD’S and Towers help, I’m going to make it! I’m proud to be part of the Towers family and to Linus Pauling (if you’re looking down) a big thank you.

Sincerly,Gary J. Rehs

## Dr. Klenner – (Intravenous) Vitamin C Paper – 1971.

Journal of Applied Nutrition Vol. 23, No’s 3 & 4, Winter 1971

Observations On the Dose and Administration of Ascorbic Acid When Employed Beyond the Range Of A Vitamin In Human Pathology

Frederick R. Klenner, M.D., F.C.C.P.

How concerned should we be about oxalic acid and kidney stones? A technical explanation.

One of the “scare” weapons used by the critics on high daily doses of ascorbic acid is the oxalic acid-kidney stone hypothesis. Meakins[36] states that the chief factors in the formation of renal calculi are perversions of metabolic processes, infection and stasis in the urinary tract.

There are two schools of thought on stone formation:

1) That there is a central nucleus of colloids on which the crystalloids are precipitated;
2) That the crystalloids are deposited from the urine in which they are present in concentrated solution, in which salt and hydrogen ion concentrations are important factors.

In all cases stasis and a concentrated urine appear to be the chief physiological factors. The only way that oxalic acid can be produced from ascorbic acid is through splitting of the lactone ring. This happens above pH5. The reaction of urine when 10 grams of vitamin C is taken daily is usually pH6.

Oxalic acid precipitates out of solution only from a neutral or alkaline solution-pH7 to pH10. Kelli and Zilva[37] reported that “Nutrition experiments showed that dehydroascorbic acid is protected in vivo from rapid transformation to the antiscorbutically impotent diketogulonic acid from which oxalic acid is derived.” Values reported in the literature for normal 24 hour urinary oxalate excretions for humans range from 14 mg to 56 mg. Lamden et al.[38] found in a group of volunteers that the ingestion of 9 grams ascorbic acid daily resulted in oxalate spills as high as 68 mg for 24 hours and in the controls without extra vitamin C the high was 64 mg for a 24 hour period.

These critics have overlooked the individual with diabetes mellitus. The amount of oxalic acid found in the diabetic patient approximates that found in the urine of a normal person taking 10 grams vitamin C each day. With the diabetic we find a paradox. Give this individual 10 grams ascorbic acid daily, by mouth, and the urinary oxalate excretion remains relatively unchanged. Diabetics are known for their diuresis. The individual who takes 10 or more grams of vitamin C each day will find that this organic compound is an excellent diuretic. No urinary stasis; no urine concentration.

The ascorbic acid kidney stone story is a myth. Methylene blue will dissolve calcium oxalate stones giving 65 mg orally 2 to 3 times a day. (Dr. M. J. Vernon Smith: Med. World News, Dec. 4, 1970)

# Diabetes mellitus response to 10 grams ascorbic acid by mouth.

Over the past 17 years we have studied the effect of 10 grams by mouth, in patients with diabetes mellitus. We found that every diabetic not taking supplemental vitamin C could be classified as having sub-clinical scurvy. For this reason they find it difficult to heal wounds. The diabetic patient will use the supplemental vitamin C for better utilization of his insulin. It will assist the liver in the metabolism of carbohydrates and to reinstate his body to heal wounds like normal individuals. We found that 60% of all diabetics could be controlled with diet and 10 grams ascorbic acid daily. The other 40% will need much less needle insulin and less oral medication. Contrary to what Medical News Letter, (Vol. 12 # 26, Dec. 25 1970) carried to the physicians the Tes-Tape is accurate in testing urine samples.

# Diabetes

Large doses of ascorbic acid do not cause diabetes mellitus in humans as has been suggested. On the contrary 10 grams daily, by mouth, has proved to be beneficial. The fact that 10 grams will allow them to heal wounds like normal individuals will save many legs in. the future. Lamden, a biochemist, instigated these fears by misinterpretation of the results reported by Patterson using the Ketone formula intravenously in rats.

# Case History: Acute Pancreatitis

Adult Male seen in the emergency room of local hospital complaining of severe, agonizing pain in the epigastrium which radiated to the back. Nausea and vomiting were present. Serum amylase studies showed a concentration of 345. This was the 4th such attack experienced by this patient. Sixty grams ascorbic acid in 700 c.c. Dextrose in water was given intravenously. 20 mg Pantapon was given in the emergency room. No additional opiates were required. The patient made an uneventful recovery. He was placed on 10 grams ascorbic acid by mouth and has not had a recurrence in almost 5 years. He has, however, developed mild diabetes mellitus which is now controlled with diet and vitamin C.

## By Mike Ciell, R.Ph. about Diabetes


Avoiding saturated fat, using “healthy” polyunsaturated oils, and building a diet on a base of carbohydrates (grains, breads, and starchy veggies) has been drummed into us by well-meaning authorities, including luminaries such as: the USDA, the American Heart Association, and the American Diabetes Association

Yet, it is a basic physiological fact that all carbohydrates are metabolized to glucose. If glucose is not used for fuel, it is automatically converted to and stored as saturated fat (only a small part-about 100 grams – will actually ever be stored as glycogen).

Vitamin C — Ascorbate or Ascorbic Acid

By now, you may have surmised that vitamin C is the lynchpin of the Unified Theory.Vitamin C, or rather the lack of sufficient ascorbate, has implications in practically every chronic disease — osteoporosis, diabetes, arthritis, cancer, macular degeneration, allergies, and chronic or re-occurring infections are just a few examples.

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