The deadly diabetes deception part 2

Greed and dishonest science has promoted a lucrative worldwide epidemic of diabetes which honesty and good science can quickly reverse by naturally restoring the body’s blood-sugar control mechanism.

As early as 1901, efforts had been made to manufacture and sell food products by the use of automated factory machinery because of the immense profits that were possible. Most of the early efforts failed because people were inherently suspicious of food that wasn’t farm fresh and because the technology was poor. As long as people were prosperous, suspicious food products made little headway.1

Margarine was introduced and was bitterly opposed by the dairy states in the US. With the advent of the Depression of the 1930s, margarine, Crisco and a host of other refined and hydrogenated products began to make significant penetration into the food markets of America. Support for dairy opposition to margarine faded during World War II because there wasn’t enough butter for the needs of both the civilian population and the military.2 At this point, the dairy industry, having lost much support, simply accepted a diluted market share and concentrated on supplying the military.

Flax oils and fish oils, which were common in the stores and considered dietary staples before the American population became diseased, have disappeared from the shelf. The last supplier of flax oil to the major distribution chains was Archer Daniels Midland, and it stopped producing and supplying the product in 1950.
More recently, one of the most important of the remaining, genuinely beneficial, fats was subjected to a massive media disinformation campaign that portrayed it as a saturated fat that causes heart failure. As a result, it has virtually disappeared from the supermarket shelves. Thus was coconut oil removed from the food chain and replaced with soy oil, cottonseed oil and rapeseed oil.3 Our parents and grandparents would never have swapped a fine, healthy oil like coconut oil for these cheap, junk oils. It was shortly after this successful media blitz that the US populace lost its war on fat.

For many years, coconut oil had been our most effective dietary weight-control agent. The history of the engineered adulteration of our once-clean food supply exactly parallels the rise of the epidemic of diabetes and hyperinsulinaemia now sweeping much of the world.

The second step to a cure for this disease epidemic is to stop believing the lie that our food supply is safe and nutritious.

The Nature of the Disease
Diabetes is classically diagnosed as a failure of the body to metabolise carbohydrates properly. Its defining symptom is a high blood-glucose level. Type I diabetes results from insufficient insulin production by the pancreas. Type II diabetes results from ineffective insulin. In both types, the blood-glucose level remains elevated. Neither insufficient insulin nor ineffective insulin can limit post-prandial (after-eating) blood sugar to the normal range. In established cases of Type II diabetes, these elevated blood sugar levels are often preceded and accompanied by chronically elevated insulin levels and by serious distortions of other endocrine hormonal markers.

The ineffective insulin is no different from effective insulin. Its ineffectiveness lies in the failure of the cell population to respond to it. It is not the result of any biochemical defect in the insulin itself. Therefore, it is appropriate to note that this is a disease that affects almost every cell in the 70 trillion or so cells of the body. All of these cells are dependent upon the food that we eat for the raw materials they need for self repair and maintenance.

The classification of diabetes as a failure to metabolise carbohydrates is a traditional classification that originated in the early 19th century when little was known about metabolic diseases or processes.4 Today, with our increased knowledge of these processes, it would appear quite appropriate to define Type II diabetes more fundamentally as a failure of the body to metabolise fats and oils properly. This failure results in a loss of effectiveness of insulin and in the consequent failure to metabolise carbohydrates. Unfortunately, much medical insight into this matter, except at the research level, remains hampered by its 19th-century legacy.
Thus Type II diabetes and its early hyperinsulinaemic symptoms are whole-body symptoms of this basic cellular failure to metabolise glucose properly. Each cell of the body, for reasons which are becoming clearer, finds itself unable to transport glucose from the bloodstream to its interior. The glucose then remains in the bloodstream, or is stored as body fat or as glycogen, or is otherwise disposed of in urine.

It appears that when insulin binds to a cell membrane receptor, it initiates a complex cascade of biochemical reactions inside the cell. This causes a class of glucose transporters known as GLUT4 molecules to leave their parking area inside the cell and travel to the inside surface of the plasma cell membrane.
When in the membrane, they migrate to special areas of the membrane called caveolae areas.5 There, by another series of biochemical reactions, they identify and hook up with glucose molecules and transport them into the interior of the cell by a process called endocytosis. Within the cell’s interior, this glucose is then burned as fuel by the mitochondria to produce energy to power cellular activity. Thus these GLUT4 transporters lower glucose in the bloodstream by transporting it out of the bloodstream into all the cells of the body.

Many of the molecules involved in these glucose- and insulin-mediated pathways are lipids; that is, they are fatty acids. A healthy plasma cell membrane, now known to be an active player in the glucose scenario, contains a complement of cis-type w=3 unsaturated fatty acids.6 This makes the membrane relatively fluid and slippery. When these cis- fatty acids are chronically unavailable because of our diet, trans- fatty acids and short- and medium-chain saturated fatty acids are substituted in the cell membrane. These substitutions make the cellular membrane stiffer and more sticky, and inhibit the glucose transport mechanism.7

Thus, in the absence of sufficient cis omega-3 fatty acids in our diet, these fatty acid substitutions take place, the mobility of the GLUT4 transporters is diminished, the interior biochemistry of the cell is changed and glucose remains elevated in the bloodstream. Elsewhere in the body, the pancreas secretes excess insulin, the liver manufactures fat from the excess sugar, the adipose cells store excess fat, the body goes into a high urinary mode, insufficient cellular energy is available for bodily activity and the entire endocrine system becomes distorted. Eventually, pancreatic failure occurs, body weight plummets and a diabetic crisis is precipitated. Although there remains much work to be done to elucidate fully all of the steps in all of these pathways, this clearly marks the beginning of a biochemical explanation for the known epidemiological relationship between cheap, engineered dietary fats and oils and the onset of Type II diabetes.

Orthodox Medical Treatment
After the diagnosis of diabetes, modern orthodox medical treatment consists of either oral hypoglycaemic agents or insulin.

• Oral hypoglycaemic agents
In 1955, oral hypoglycaemic drugs were introduced. Currently available oral hypoglycaemic agents fall into five classifications according to their biophysical mode of action.8 These classes are: biguanides; glucosidase inhibitors; meglitinides; sulphonylureas; and thiazolidinediones.

The biguanides lower blood sugar in three ways. They inhibit the normal release by the liver of its glucose stores, they interfere with intestinal absorption of glucose from ingested carbohydrates, and they are said to increase peripheral uptake of glucose.

The glucosidase inhibitors are designed to inhibit the amylase enzymes produced by the pancreas and which are essential to the digestion of carbohydrates. The theory is that if the digestion of carbohydrates is inhibited, the blood sugar level cannot be elevated.

The meglitinides are designed to stimulate the pancreas to produce insulin in a patient that likely already has an elevated level of insulin in their bloodstream. Only rarely does the doctor even measure the insulin level. Indeed, these drugs are frequently prescribed without any knowledge of the pre-existing insulin level. The fact that an elevated insulin level is almost as damaging as an elevated glucose level is widely ignored.

The sulphonylureas are another pancreatic stimulant class designed to stimulate the production of insulin.

Serum insulin determinations are rarely made by the doctor before he prescribes these drugs. They are often prescribed for Type II diabetics, many of whom already have elevated ineffective insulin. These drugs are notorious for causing hypoglycaemia as a side effect.

The thiazolidinediones are famous for causing liver cancer. One of them, Rezulin, was approved in the USA through devious political infighting, but failed to get approval in the UK because it was known to cause liver cancer. The doctor who had responsibility to approve it at the FDA refused to do so. It was only after he was replaced by a more compliant official that Rezulin gained approval by the FDA.

It went on to kill well over 100 diabetes patients and cripple many others before the fight to get it off the market was finally won.

Rezulin was designed to stimulate the uptake of glucose from the bloodstream by the peripheral cells and to inhibit the normal secretion of glucose by the liver. The politics of why this drug ever came onto market, and then remained in the market for such an unexplainable length of time with regulatory agency approval, is not clear.9 As of April 2000, lawsuits commenced to clarify this situation.10

• Insulin
Today, insulin is prescribed for both the Type I and Type II diabetics. Injectable insulin substitutes for the insulin that the body no longer produces. Of course, this treatment, while necessary for preserving the life of the Type I diabetic, is highly questionable when applied to the Type II diabetic. It is important to note that neither insulin nor any of these oral hypoglycaemic agents exerts any curative action whatsoever on any type of diabetes. None of these medical strategies is designed to normalise the cellular uptake of glucose by the cells that need it to power their activity. The prognosis with this orthodox treatment is increasing disability and early death from heart or kidney failure or the failure of some other vital organ.

Alternative Medical Treatment
The third step to a cure for this disease is to become informed and to apply an alternative methodology that is soundly based upon good science.
Effective alternative treatment that directly leads to a cure is available today for some Type I and for many Type II diabetics. About 5% of the diabetic population suffers from Type I diabetes; about 95% has Type II diabetes.11 Gestational diabetes is simply ordinary diabetes contracted by a woman who is pregnant.

For the Type I diabetic, an alternative methodology for the treatment of Type I diabetes is now available. It was developed in modern hospitals in Madras, India, and subjected to rigorous double-blind studies to prove its efficacy.12 It operates to restore normal pancreatic beta cell function so that the pancreas can again produce insulin as it should. This approach apparently was capable of curing Type I diabetes in over 60% of the patients on whom it was tested. The major complication lies in whether the antigens that originally led to the autoimmune destruction of these beta cells have disappeared from or remain in the body. If they remain, a cure is less likely; if they have disappeared, the cure is more likely.

The goal of any effective alternative program is to repair and restore the body’s own blood-sugar control mechanism. It is the malfunctioning of this mechanism that, over time, directly causes all of the many debilitating symptoms that make orthodox treatment so financially rewarding for the diabetes industry.

For Type II diabetes, the steps are:
• Repair the body’s faulty blood sugar control system. This is done simply by substituting clean, healthy, beneficial fats and oils in the diet for the pristine-looking but toxic trans-isomer mix found in attractive plastic containers on supermarket shelves. Consume only flax oil, fish oil and occasionally cod liver oil until blood sugar starts to stabilise. Then add back healthy oils such as butter, coconut oil, olive oil and clean animal fat.
Read labels; refuse to consume cheap junk oils when they appear in processed food or on restaurant menus. Diabetics are chronically short of minerals; they need to add a good-quality, broad-spectrum mineral supplement to the diet.

• Control blood sugar manually during the recovery cycle. Under medical supervision, gradually discontinue all oral hypoglycaemic agents along with any additional drugs given to counteract their side effects.
Develop natural blood-sugar control by the use of glycaemic tables, by consuming frequent small meals (including fibre-rich foods), by regular post-prandial exercise, and by the complete avoidance of all sugars along with the judicious use of only non-toxic sweeteners.13 Avoid alcohol until blood sugar stabilises in the normal range. Keep score by using a pinprick-type glucose meter. Keep track of everything you do with a medical diary.

• Restore a proper balance of healthy fats and oils when the blood sugar controller again works. Permanently remove from the diet all cheap, toxic, junk fats and oils as well as the processed and restaurant foods that contain them. When the blood sugar controller again starts to work correctly, gradually introduce additional healthy foods to the diet. Test the effect of these added foods by monitoring blood sugar levels with the pinprick-type blood sugar monitor. Be sure to include the results of these tests in your diary also.

• Continue the program until normal insulin values are also restored after blood sugar levels begin to stabilise in the normal region. Once blood sugar levels fall into the normal range, the pancreas will gradually stop overproducing insulin. This process will typically take a little longer and can be tested by having your physician send a sample of your blood to a lab for a serum insulin determination.
A good idea is to wait a couple of months after blood sugar control is restored and then have your physician check your insulin level. It’s nice to have blood sugar in the normal range; it’s even nicer to have this accomplished without excess insulin in the bloodstream.

• Separately repair the collateral damage done by the disease. Vascular problems caused by a chronically elevated glucose level will normally reverse themselves without conscious effort. The effects of retinopathy and of peripheral neuropathy, for example, will usually self repair. However, when the fine capillaries in the basement membranes of the kidneys begin to leak due to chronic high blood glucose, the kidneys compensate by laying down scar tissue to prevent the leakage. This scar tissue remains even after the diabetes is cured, and is the reason why the kidney damage is not believed to self repair.

A word of warning
When retinopathy develops, there may be a temptation to have the damage repaired by laser surgery. This laser technique stops the retinal bleeding by creating scar tissue where the leaks have developed. This scar tissue will prevent normal healing of the fine capillaries in the eye when the diabetes is reversed.

By reversing the diabetes instead of opting for laser surgery, there is an excellent chance that the eye will heal completely. However, if laser surgery is done, this healing will always be complicated by the scar tissue left by the laser. The arterial and vascular damage done by years of elevated sugar and insulin and by the proliferation of systemic candida will slowly reverse due to improved diet.

Arterial damage can be reversed much more quickly by using intravenous chelation therapy.14 What would normally take many years through diet alone can often be done in six months with intravenous therapy. This is reputed to be effective over 80% of the time. For obvious reasons, don’t expect your doctor to approve of this, particularly if he’s a heart specialist.

Recovery Time
The prognosis is usually swift recovery from the disease and restoration of normal health and energy levels in a few months to a year or more. The length of time that it takes to effect a cure depends upon how long the disease was allowed to develop.
For those who work quickly to reverse the disease after early discovery, the time is usually a few months or less. For those who have had the disease for many years, this recovery time may lengthen to a year or more. Thus, there is good reason to get busy reversing this disease as soon as it becomes clearly identified.
By the time you get to this point in this article, and if we’ve done a good job of explaining our diabetes epidemic, you should know what causes it, what orthodox medical treatment is all about, and why diabetes has become a national and international disgrace.
Of even greater importance, you have become acquainted with a self-help program that has demonstrated great potential to actually cure this disease.

About the Author:
Thomas Smith is a reluctant medical investigator, having been forced into curing his own diabetes because it was obvious that his doctor would not or could not cure it. He has published the results of his successful diabetes investigation in his self-help manual, Insulin: Our Silent Killer, written for the layperson but also widely valued by the medical practitioner.

1. Trager, J., The Food Chronology, Henry Holt & Company, New York, 1995 (items listed by date)
2. “Margarine”, Encyclopedia Americana, Library Edition, vol. 9, 1966, pp. 279-280
3. Fallon, S., Connolly, P., Enig, M.C., Nourishing Traditions, Promotion Publishing, 1995;
Enig, M.C., Coconut: In Support of Good Health in the 21st Century
4. Houssay, Bernardo, A., MD, et al., Human Physiology, McGraw-Hill Book Company, 1955, pp. 400-421
5. Gustavson, J., et al., Insulin-stimulated glucose uptake involves the transition of glucose transporters to a caveolae-rich fraction within the plasma cell membrane: implications for Type II Diabetes, Mol. Med. 2(3):367-372 (May 1996)
6. Ganong, William F., MD, Review of Medical Physiology, 19th edition, 1999, p. 9, pp. 26-33
7. Pan, D.A. et al., Skeletal muscle membrane lipid composition is related to adiposity and insulin action, J. Clin. Invest. 96(6):2802-2808 (December 1995)
8. Physicians’ Desk Reference, 53rd edition, 1999
9. Smith, Thomas, Insulin: Our Silent Killer, Thomas Smith, Loveland, Colorado, revised 2nd edition, July 2000, p. 20
10. Law Offices of Charles H. Johnson & Associates
11. American Heart Association, Diabetes Mellitus Statistics,
12. Shanmugasundaram, E.R.B. et al., Possible regeneration of the Islets of Langerhans in Streptozotocin-diabetic rats given Gymnema sylvestre leaf extract, J. Ethnopharmacology 30:265-279 (1990);
Shanmugasundaram, E.R.B. et al., Use of Gemnema sylvestre leaf extract in the control of blood glucose in insulin-dependent diabetes mellitus, J. Ethnopharmacology 30:281-294 (1990)
13. Many popular artificial sweeteners on sale in the supermarket are extremely poisonous and dangerous to the diabetic; indeed, many of them are worse than the sugar the diabetic is trying to avoid; see, for example, Smith, ibid., pp. 53-58.
14. Walker, Morton, MD, and Shah, Hitendra, MD, Chelation Therapy, Keats Publishing, Inc., New Canaan, Connecticut, 1997, ISBN 0-87983-730-6