What Are We Doing To Ourselves?

In the fall of 1997, the Centers for Disease Control confirmed that the number of Americans living with diabetes has skyrocketed in the past 40 years with a record sixfold increase in this chronic disease since 1958.

It is estimated that nearly 16 million Americans are suffering with diabetes and 5 million more may have it but not know it. There are two types of diabetes mellitus: Type I, called insulin-dependent juvenile diabetes, and Type II, called adult-onset diabetes. The incidence of both has skyrocketed over the last 50 years. It is directly attributable to what we trumpet as modern living.

Over the past four decades, intensive national mass vaccination campaigns have dramatically increased vaccination rates among American children who now recieve 34 doses of ten different viral and bacterial vaccines before they enter kindergarten. Recently published data in medical journals suggest that the increasing number of childhood vaccines may be playing a role in the big jump in the number of cases of Type I or juvenile diabetes.

In order to understand Type II it is essential to have a working knowledge of its precursor, the beginning and defining indicator of adult onset diabetes. Hyperinsulinemia is the presence of excess insulin in the blood stream; this abnormal condition causes excess cholesterol, atherosclerosis, heart failure, impotence, stroke and eventually Type II diabetes.

High insulin levels appear in the diabetic blood stream long before high glucose levels do yet high glucose remains the classic diabetes symptom. Insulin levels are rarely, if ever, used as a diabetic marker except by research scientists.

WHAT IS DIABETES?

Both Types I and II diabetes are considered diabetes mellitus, a chronic degenerative disease caused when the pancreas either fails to produce a protein hormone called insulin or the body’s cells are resistant to the action of insulin.

Without insulin, the body cannot process and use glucose, a blood sugar which is a chief source of energy for living organisms and is found in certain foods like fruit. If the body’s cells have become resistant to insulin, glucose cannot be moved from the blood to cells in order to be transformed into energy.

Type I diabetes, also called insulin-dependent diabetes mellitus or IDDM, occurs mostly in children and young adults. They represent ten percent of diabetes diagnoses. In Type I diabetes, the body cannot produce insulin.

This causes glucose to build up in the bloodstream and be secreted from the body in the urine, leaving the body to starve for energy because the body’s cells cannot get the necessary nourishment provided by glucose. Symptoms include excessive thirst, hunger, urination, dehydration and often weight loss. Insulin injections must be taken daily to keep blood glucose levels stable.

Type II Diabetes

Type II diabetes occurs primarily in middle age and makes up almost 90 percent of all diagnosed cases of diabetes. The pancreas still produces insulin in Type II diabetes but the body’s cells are resistant to the action of insulin and glucose is not absorbed properly by the cells. Obesity and a family history of diabetes are risk factors for Type II diabetes.

Exercise, weight control, diet restrictions and medication can be used to control Type II diabetes in many cases. Temporary insulin injections may also be given.

Diabetes Type I and II are chronic diseases that can become progressively debilitating for the individual as time goes on. When uncontrolled or inadequately controlled, diabetes leads to blindness, loss of hearing, heart and kidney disease, strokes, cataracts, nerve damage, paralysis of the intestinal tract or gangrene requiring amputation of limbs and death.

There have been estimates that some 125 million people worldwide have diabetes and that this number is expected to double by the year 2025. According to the CDC, nearly 800,000 new cases of diabetes are diagnosed in the US every year, with about 6 percent of the US population now thought to have the disease.

Diabetes is the nation’s seventh leading cause of death and kills or is a co-factor in the deaths of some 200,000 Americans every year. The leading cause of acquired blindness, diabetes contributes to about 24,000 new cases of acquired blindness in the US every year.

Half of all amputations performed in the US are caused by diabetes, which means that about 54,000 amputations are diabetes-related. Diabetes is the leading cause of kidney failure and the need for dialysis and kidney transplants. Between 1980 and 1994, diabetes rose by 33 percent among black Americans and 11 percent among white Americans.

Costs to cope with the growing epidemic of diabetes are high. In 1992, it was estimated that diabetes cost the US $85 billion for medical treatment and an additional $47 billion for lost work time, disability payments and premature death.

DIABETES MELLITUS

The pancreas is called the "hidden organ" because it is located deep in the abdomen behind the stomach. About six to eight inches long in the adult, the organ contains thin tubes that come together like the veins of a leaf. These tubes join to form a single opening into the intestine that is located just beyond the stomach.

The pancreas produces juices and enzymes that flow through these tubes into the intestine where they mix with food. The enzymes digest fat, protein, and carbohydrates so they can be absorbed by the intestine. Pancreatic juices, therefore, play an important role in maintaining good health. The pancreas also produces insulin, which is picked up by the blood flowing through the organ. Insulin is important in regulating the amount of sugar or glucose in the blood.

Many cases of diabetes are caused by a deficiency of insulin. Insulin is needed to help glucose, which is a major source of energy, enter the body’s cells. It is not known why insulin producing cells in the pancreas die off. When they cease to function, glucose accumulates in the blood and eventually spills into the urine. These patients require daily insulin injections.

More importantly, high blood glucose levels over time result in significant changes in blood vessels in the eyes, kidneys, heart, legs, and nerves. Damage to these vital organs represents the major risk for patients with diabetes.

Other patients who develop diabetes later in life seem to have sufficient insulin in the pancreas, but for some unknown reason it is not available for the body’s use. These patients typically are overweight and, therefore, weight loss is critical for them. In addition, oral medications can be taken that help release insulin from the pancreas. All diabetics need to maintain normal or near normal blood glucose levels to prevent or delay the complications of this disease.

The special cells in the pancreas, called the Islets of Langerhans, produce insulin and secrete it into the blood stream. Insulin is the primary regulator of carbohydrate metabolism in the body. When we eat simple carbohydrates (sugars) they are absorbed directly into the blood stream relatively quickly.

When we eat complex carbohydrates (starches and others), it is digested (broken down) into its component smaller units and eventually into glucose, which is then absorbed into the bloodstream. The pancreas senses the level of glucose in the blood and produces insulin accordingly.

Insulin then helps the glucose enter the cells, where it is used for energy production. If too much insulin is produced, not enough glucose remains in the blood and if too little is produced, too much glucose remains in the blood and not enough enters the cells.

If the pancreas is overworked and does not receive the nutrients it needs to maintain its own healthy metabolic processes, it can become exhausted and not produce enough insulin. The result is diabetes. If on the other hand, too much insulin is produced, the blood sugar level will be too low. This condition is called hypoglycemia. Therefore, maintaining the proper balance is important.

JUVENILE DIABETES AND VACCINATION:

Doctors started making reports in the medical literature as early as 1949 that some children injected with pertussis (whooping cough) vaccine (now part of the DPT or DTaP shot) were having trouble maintaining normal glucose levels in their blood. Lab research has confirmed that pertussis vaccine can cause diabetes in mice.

As diabetes research progressed in the 1960’s, 70’s and 80’s, there were observations that viral infections may be a co-factor in causing diabetes. The introduction of live virus vaccines, such as live MMR vaccine which is made from weakened forms of the live measles, mumps and rubella viruses, has raised questions about whether live vaccine virus could be a co-factor in causing chronic diseases such as diabetes.

One virus, the rubella virus, has already been shown to be associated with diabetes. Babies infected with the rubella virus in their mother’s womb, who are born with congenitally acquired rubella syndrome, often develop Type I diabetes. One 1980 study concluded that rubella virus can infect pancreatic islet cells and that the infection can severely reduce levels of secreted insulin. Another study in the 1980’s demonstrated that, after live rubella vaccination, the rubella virus can persist in the body of a vaccinated person for many years.

Like rubella, mumps disease has been strongly associated with the development of Type I diabetes. Like the rubella virus, the mumps virus can infect pancreatic islet cells. And like the live rubella vaccine, there are persistent reports in the medical literature that some children develop diabetes after receiving live mumps vaccine.

An accumulation of scientific research today suggests that Type I diabetes is an auto-immune disease. Auto-immunity is created when the immune system malfunctions and attacks its own body. Genetic predisposition and environmental factors such as a viral infection are thought to be co-factors in the development of auto-immune disease, including diabetes.

Because a vaccine artificially manipulates the immune system in order to make it act as if it has recovered from and is immune to a particular disease, some scientists are investigating whether vaccination can be a cofactor in the development of auto-immune diseases like diabetes. This research is particularly important for individuals who may have a genetic predisposition to auto-immunity, such as those with a family history of auto-immune disease.

MORE VACCINES EQUAL MORE DIABETES

Evidence of a vaccination diabetes connection has been strengthened since 1996 by the epidemiologic investigation of J. Barthelow Classen, M. D., a former researcher at the National Institutes of Health and the founder and CEO of Classen Immunotherapies, Inc.. Dr. Classen is developing ways to prevent auto-immune disease and maintains that one reason there is a growing epidemic of diabetes in the world is because vaccines given to children at two months and older can induce immune-mediated diabetes.

Classen has analyzed mass vaccination and disease incidence data from foreign countries, which keep better records of diabetes incidence than the U.S., as well as conducting basic science research experiments on mice and rats to support his argument.

Beginning with lab experiments, he demonstrated that 8 week old rats and mice injected with DPT vaccine had a higher incidence of diabetes than those who were not injected with DPT vaccine at 8 weeks old. Then he searched for evidence in existing epidemiological data on human populations to suggest that injecting two month old babies with vaccines causes an increased incidence in diabetes.

In the May 24, 1996 New Zealand Medical Journal, Dr. Classen reported that there was a 60 percent increase in Type I diabetes or juvenile diabetes following a massive campaign in New Zealand from 1988 to 1991 to vaccinate babies six weeks of age or older with hepatitis B vaccine.

His analysis of a group of 100,000 New Zealand children followed since 1982 showed that the incidence of diabetes before the hepatitis B vaccination program began in 1988 was 11.2 cases per 100,000 children per year while the incidence of diabetes following the hepatitis B vaccination campaign was 18.2 cases per 100,000 children per year. This represents a 62% increase.

In the October 22, 1997 issue of Infectious Diseases in Clinical Practice, Classen presented more data further substantiating his findings of a vaccine-diabetes connection. He reported that the incidence of diabetes in Finland was stable in children under 4 years of age until the government made several changes in its childhood vaccination schedule.

In 1974, 130,000 children aged 3 months to 4 years were enrolled in a vaccine experimental trial and injected with Hib vaccine or meningococcal vaccine. Then, in 1976, the pertussis vaccine used in Finland was made stronger by adding a second strain of bacteria. During the years 1977 to 1979, there was a 64 percent increase in the incidence of Type I diabetes in Finland compared to the years 1970 to 1976.

In 1982, another vaccine was added to the childhood vaccination schedule in Finland. Children aged 14 months to six years were given the live MMR (measles-mumps-rubella) vaccine. This was followed by the injection of 114,000 Finnish children aged 3 months and older with another experimental Hib vaccine. In 1988, Finland recommended that all babies be injected with the Hib vaccine.

The introduction of the new vaccines in Finland was followed by a 62 percent rise in the incidence of diabetes in the 0 to 4 year old age group. It was also accompanied by a 19 percent rise of diabetes in the 5 to 9 year old age group between the years 1980 and 1982 and 1987 and 1989. Classen concluded: "The net effect was the addition of three new vaccines to the 0-4 year old age group and a 147 percent increase in the incidence of IDDM - insulin dependent diabetes mellitus.

The addition of one new vaccine to the 5-9 year olds and a rise in the incidence of diabetes of 40 percent, and no new vaccines added to the 10 to 14 year olds and a rise in the incidence of IDDM by only 8 percent between the intervals 1970-1976 and 1990-1992. The rise in IDDM in the different age groups correlated with the number of vaccines given."

Although more than $l billion dollars is appropriated by Congress to federal health agencies every year to develop, purchase and promote the mass use of vaccines by American children, none of that money is used to fund independent vaccine researchers to investigate vaccine-associated health problems like diabetes. In fact, reputable researchers outside of government like Dr. Classen, who want to do vaccine adverse event research, are not given government grants to do that kind of research.

The National Vaccine Information Center maintains that there is an inherent conflict of interest in allowing the same health officials in federal agencies who are responsible for researching, developing, regulating, making national policy for and promoting vaccines to also be in control of monitoring vaccine reactions and evaluating health problems associated with vaccines.

There is a similar conflict of interest in relying solely on scientific data supplied by drug companies, who make and sell vaccines for a profit, to license vaccines safe for use by the public without corroborating independent scientific data about the vaccine’s safety.

"Health officials in federal agencies have no accountability to anyone when it comes to setting priorities for how our tax dollars are used when it comes to vaccine research," said NVIC president and co-founder Barbara Loe Fisher. "They can choose to do whatever they want to do with the money they get from Congress.
They choose to ignore the mounting evidence that vaccines are playing a role in the current epidemic of chronic disease, such as diabetes, in our society. Instead, our tax money is used to create more vaccines to add to the mandatory vaccination schedule for our children.

There have never been and there are no plans to fund large independent studies to back-up the scientific validity of the government’s current vaccine policies and independently confirm they are safe." NVIC is located at 512 W Maple Ave #206; Vienna, VA 22180 (703) 938-DPT3.

Other theories contend that a significant factor contributing to the dramatic increase in Type I diabetes are being exposed to the same dietary habits that cause Type II diabetes in adults as the fetus is exposed to the dietary habits of the mother via the womb.

Additionally some think that there is a protein present present in cow’s milk that closely mimics the beta cells in the pancreas which are responsible for producing insulin. When the body mobilizes antibodies to neutralize these foreign invaders they also harm the beta cells and thereby impair the blood sugar control system of the body.

Insulin The Silent Killer

Hyperinsulinemia, which is characterized by elevated levels of insulin and glucose, and Type II diabetes together with the related diseases of the arterial and vascular system, constitute a hidden epidemic that is implicated in over 40% of the annual deaths from all causes.

Type II diabetes alone affects between 10% and 20% of the population. This is up from 0.0028% of the same population in the 1880’s. Hyperinsulinemia appears to be directly caused by the re-engineering of our once natural food supply. Essential nutrients have been removed from our food for the purpose of extending its shelf life. The average American consumes 37 pounds of sugar annually.

This two stage assault upon our health has proven deadly, some countries have banned certain American foods, and still others are currently considering a ban, because of specifically identified health hazards of American food manufacture that remain effectively unregulated by any government agency.

These conditions can be reversed by reversing the changes that caused them to begin with. It is likely that it is no longer necessary to become dependent on any artificial drug. In the beginning the defining symptom of hyperinsulinemia is the presence of excess insulin in the blood stream; this abnormal condition causes excess cholesterol, atherosclerosis, heart failure, impotence, stroke and eventually Type II diabetes.

High insulin levels appear in the diabetic blood stream long before high glucose does; yet high glucose remains the classic diabetes symptom. Insulin levels are rarely, if ever, used as a diabetic marker except by research scientists.

In 1949, when our hyperinsulinemia epidemic really started to take off, atherosclerosis, heart failure, stroke and impotence were understood to be symptoms of diabetes. When this epidemic became recognized, the medical attack on the disease included a reclassification of it into several diseases according to symptoms.

When we cure hyperinsulinemia, we also enormously reduce our chances of Type II diabetes, atherosclerosis, heart attack, stroke and impotence. Increasingly cancer is implicated in this causal relationship, but in this, the evidence is not yet fully compelling.

FAILURE OF THE BLOOD SUGAR CONTROL SYSTEM (BSCS)

The human body has a complex mechanism to control the amount of glucose in the blood to within very tight limits. This mechanism is called the blood sugar control system (BSCS). It functions by using insulin to decrease the blood sugar that has become elevated by eating.

It increases the blood sugar during fasting by the use of glucagon. This BSCS operates this way to deliver the correct amount of insulin into the blood stream and to minimize the rise of glucose after we eat. An excess of glucose or an excess of insulin in the blood stream will cause damaged blood vessels.

These damaged blood vessels then cause the whole shopping list of medical specialty diseases that currently afflict Americans. This BSCS, like any control system, has a number of failure modes. Which mode is involved in a particular disease event depends on what part of the BSCS has failed.

The treatment for one BSCS problem may not be effective for another, or even worse, may be counter productive, In the case of hyperinsulinemia, insulin loses its effectiveness. Hyperinsulinemia causes the body to compensate for the loss of effectiveness of insulin by increasing its pancreatic secretion of insulin.

This hyperinsulinemia is the direct preciptating cause of Type II diabetes, stroke, atherosclerosis, heart failure, male impotence, neuropathy, kidney failure, diabetic gangrene, liver damage and many other diseases of impaired circulation.

Hyperinsulinemia is the disease that is the precursor to all of the rest of these diseases as well as many others not specifically mentioned. They spring from the arterial and vascular damage done to our circulatory system by excess insulin and the corresponding excess glucose that will eventually manifest.

Insulin is manufactured by our pancreas. It is released into our blood stream by a hormone control system that carefully meters out the required amount when our blood glucose rises after eating. The purpose of insulin is to sweep the glucose from our blood stream into our body cells where it is used for energy. When afflicted by Hyperinsulinemia our blood stream remains at elevated levels of both insulin and glucose. This is what causes arterial and vascular damage.

Insulin is also a synthetic manufactured product. It may be obtained in quick acting, intermediate and slow acting forms. Insulin has often been prescribed to treat the symptomatic high glucose levels associated with Type II diabetes. Since much of the damage caused by Type II diabetes is caused by excess insulin, this treatment is not only incorrect, it can also be very damaging.

The appropriate reason to prescribe insulin is when the insulin level is low; not, when the glucose is high. Furthermore, one of the earliest indicators of incipient Type II diabetes is elevated insulin levels. This often occurs before elevated blood glucose levels are evident. When in doubt, require that the attending physician obtain a GITT before prescribing insulin. A GITT is a glucose and insulin tolerance test.

Hyperinsulinemia is actually a lifestyle disease of fatty degeneration, excess sugar and nutritional deficiency. It is most often curable by correcting the lifestyle that causes it. This is a surprisingly easy and straightforward process. It simply requires us to understand what is in the food that we eat and what this food does to our bodies.

Modern medical research identifies Hyperinsulinemia as showing the abnormal blood insulin and glucose levels associated with diabetes together with vascular damage, atherosclerosis, impotence and neuropathy. Diabetes may exhibit either unusually high or low insulin levels together with a high blood glucose level depending upon which particular malfunction of the BSCS is causing the problem.

Because of the differing forms of diabetes, it is vital to diagnose each specific case prior to determining a treatment protocol. It is also desirable to exclude a number of non diabetes look a likes from consideration through careful diagnosis. This is best done by blood and urine laboratory work under medical supervision.

yperinsulinemia is, by far, the major blood sugar control system failure mechanism in this country.

A responsible diagnosis must exclude the other BSCS failures as well as the diabetes look-a-likes before embarking upon a course of treatment, Since the 1940’s, when Hyperinsulinemia exploded upon the scene, the vast majority of diabetic cases in this country have been, and are now, Type II diabetes.

Some of the other diabetes forms and the diabetic look alike diseases are: renal glycosauria, fructosauria, pentosauria, hereditary fructose intolerance and diabetes insipidus. The importance of appropriate diagnosis in the treatment process makes it easier to successfully treat a disease that is correctly identified.

IN SIMPLE TERMS

Every cell in our body exists as a discrete organism in an overall organism called the body. The body provides a nutrient bath that allows them to survive and to thrive with adequate glucose. Each cell must independently be able to obtain from this bath the vital nutrients that it requires to function.

Some cells, adipose cells, merely store fat; others like heart muscle, must be able to perform useful work to sustain the body as a whole. Waste, excreted by these cells, as a result of their metabolic activity, is carried away by another cellular bath called the lymph system, which is a sort of cellular sewer system. Although this is also vital to cellular health, it is not of fundamental importance to understanding Hyperinsulinemia.

When insulin, a powerful anabolic hormone, is emitted into the blood stream by the beta cells of the pancreas, it normally affects the membranes of every cell in our body to cause a variety of different activities. In adipose tissue fat is stored, in the liver glycogen is stored and in most other tissue glucose is transported through the cell plasma membrane to be used as fuel by the cell.

The normal trigger, that causes the insulin to be emitted into the blood stream, is the presence of glucose in the portal vein being detected by the pancreas. This occurs when we eat carbohydrates. When glucose is present in sufficient amounts, the pancreas beta cells emit insulin.

When the glucose level in the portal vein falls to a sufficiently low value the pancreas emits glucagon from its alpha sites. This glucagon stimulates the liver to release stored glucose into the blood stream. The liver subsequently does this by converting its stored glycogen into glucose and releasing it into the blood stream. It is in this way that these two pancreatic sites, alpha and beta, correct for a blood sugar that is too low or too high.

When a person is stressed or involved in a fear reaction, this normal glucose control mechanism is overridden by the adrenal glands. The adrenal emits adrenaline and noradrenaline, (epinephrin and norepinephrin), to prepare the body for a fight or flight situation. One of the functions of the adrenaline is to stimulate the emission of glucose from the glycogen stores in the liver. It does this by stimulating the pancreas to emit glucagon.

Insulin also acts to convert about 30% of the glucose, from the carbohydrates in the food that we eat, into glycogen for storage in the liver. This constitutes the stored reserves of glucose for subsequent use when the body may not have an immediate food supply from which to derive glucose.

This can occur during fasting. It can also occur due to an unexpectedly large demand for energy usage by the body; as, perhaps, in an emergency as indicated above. This is a relatively short term rapidly accessed glucose stored supply.

In addition to these two mechanisms for the clearing of new glucose from the bloodstream, insulin also acts as a long term lipolytic agent to process some of the glucose, along with some of the fats and proteins, into fat which is then stored throughout the body in adipose cells. This is a relatively long term slowly accessed energy supply.

Thus, there are these three primary methods in which insulin in the normal non-diabetic blood sugar control system functions to clear the periodic high blood glucose concentrations from the bloodstream when we eat. This whole area of medical knowledge is undergoing rapid change as the blood sugar control system is becoming better understood.

CHOLESTEROL and TYPE II DIABETES

Much has been made, in the pop medical literature, about the need to reduce cholesterol in the diet. Unfortunately much of this misleading information doesn’t even hint at the insulin connection to the cholesterol problem. Approximately 85% of the store of cholesterol in our bodies is manufactured by our liver.

Cholesterol is a vital nutrient used in the construction of cellular membranes, brain cells, nerve sheaths and many other necessary components of our body. About 15% of our cholesterol comes from our diet. To attempt to reduce the cholesterol level by reducing our dietary cholesterol is like trying to empty the ocean with a teaspoon; it is extremely ineffective.

Through a well understood chain of events, insulin increases LDL the so called bad fats. It also decreases the production of HDL, the so called good fats, by inhibiting the activity of the enzyme lipoprotein lipase. This produces a decrease in HDL and an increase in serum triglycerides.

Both of these are markers for arterial damage and atherosclerosis. LDL normally conveys newly manufactured cholesterol from the liver to the rest of the body through the blood stream. HDL normally conveys cholesterol from the blood stream to the liver for recycling and disposal.

With hyperinsulinemia, excess insulin in the blood stream, as in Type II diabetes, normal cholesterol is produced but the body mechanism for keeping it in check does not function very well. Triglycerides are elevated and the LDL to HDL ratio is distorted in a diseased direction.

A diagnosis of high cholesterol should be viewed as a need to test for high insulin level and should be viewed as a probable indicator of incipient Hyperinsulinemia and Type II diabetes.

Hyperinsulinemia will occur much earlier than hyperglycemia. Hypercholesterolemia is a reasonable early warning of the possible onset of this disease. In addition to the upsetting action that high insulin levels have on the cholesterol balance, it is also implicated in other disorders of fat metabolism and dietary fat ingestion as well as venous and arterial damage. Type II diabetes is a disease of fat metabolism and circulatory damage just as much as of carbohydrate metabolism.

Hyperinsulinemia is becoming recognized as producing a form of diabetes that is characterized by adequate, often excess insulin; however the insulin in this Type II diabetic doesn’t seem work to sweep the glucose from the bloodstream. Thus it has become known as the "insulin resistant" form of diabetes or Hyperinsulinemia.

CELLULAR FUNCTION

It was thought that insulin, by acting on the plasma membrane cell receptors, directly facilitated the passage of glucose from the blood plasma in the vicinity of the cell to its interior. It was thought to do this by binding to the glucose molecules in the blood stream, thereby changing their shape and electrical potential to facilitate this passage through the membrane receptor into the cell interior.

The analogy to a lock and key relationship is very descriptive. In the Type II diabetic it is precisely this mechanism for transporting glucose into the cell that does not seem to work correctly. Therefore the cell must have alternate means of gaining sustenance.
There is a backup system that allows our cells to burn short and medium chain fatty acids. These fatty acids appear in the blood stream from digestive action in the duodenum and from insulin mediated fatty acid synthesis in our liver.

Our cells have the ability to burn glucose when it is available and these fatty acids when glucose is not available. This burning of fatty acids is not without its adverse consequences. In addition to the primary pathways discussed, there are other pathways that our body uses as alternate and backup mechanisms to ensure the nourishment of our cells.

For example, in addition to the synthesis of glucose from fatty acids we also have an ability to "burn" amino acids in the protein that we eat. This is a last resort method that the body uses when all others fail. This pathway generates ammonia as a waste product in our cellular metabolism.

Ammonia, a damaging biological chemical, must be transformed into water soluble urea for excretion. This is done by the liver. Excessive conversion of ammonia to urea is potentially damaging to the liver. It is for this reason the Hyperinsulinemic or the diabetic must be careful about eating a high protein diet over a long period of time.
The cell, using any one or more of these pathways to obtain fuel, "burns" this fuel in its internal mitochondria engine to produce ATP. It is this ATP that supplies the energy used by the cell. The cell is then able to repair any damage it may have; it is then able to replicate and to perform the work for which it was designed.

For example, a pancreatic cell may make insulin, a heart cell may pump blood, a lung cell may absorb oxygen or a stomach cell may emit hydrochloric acid. Brain cells and nerve cells are unique in that they require glucose only; they lack the capability to "burn" fatty acids and proteins. That is why we sometimes get dizzy from low blood pressure or hypoglycemia when the glucose concentration in the blood plasma near the brain cells becomes low.

HYPERINSULINEMIA AND THE TYPE II DIABETES SYNDROME

The incidence of diabetes in the general population was 2.8 cases per 100,000 people in 1880. It rose to 29.7 cases per 100,000 people in 1949. In 1949, the manner of keeping statistics was changed and the subsequent results are no longer directly comparable.

If the 1949 statistic is recomputed by the new method 29.7 cases per 100,000 becomes 16.4 per 100,000. Clearly the new method of tracking this disease results in the apparent decline in the incidence of it. Prior to 1949, diabetes was defined according to the microvascular, vascular and arterial symptoms that it produced as well as by the loss of control of blood sugar.

After 1949, the vascular and arterial diseases were separately categorized. A major effect of this paperwork change was to obscure the incredible rise in the incidence of the disease and to open up some additional medical specialties.

The National Diabetes Information Clearinghouse estimates today’s incidence of diabetes at 15.7 million cases or about 9% of the 174 million surveyed in their database. Extrapolating this to our 260 million population yields a combined total of 23.5 million people affected with this disastrous disease. About 2/3 of these cases have been diagnosed and about 1/3 are suffering with the disease without realizing that they have it. These numbers, remember, are being calculated under the new system.

Other observers estimate that today diabetes affects 20,000 people out of every 100,000 with about 10,000 out of 100,000 being moderately to severely debilitated. If we compute the death rate from diabetes by using data from American Demographics for the year 1995 and use the pre-1949 method we obtain a diabetes toll that accounts for over 40% of all deaths for 1995. It is evident that statistical manipulation and redefinition of the disease have obscured its epidemic nature.

Thus in the space of 100 years, diabetes has gone from 0.0028% to 20% of the population. This means that today we have 6,900 diabetes cases for each one that we had two generations ago. Today no doctor is unfamiliar with its symptoms. In 1880, the disease was so rare that few doctors ever saw it and many could not recognize it. Even with the new classification that minimizes its apparent incidence, diabetes is listed in the top ten leading causes of misery and death; and, it is known to be a precursor to at least two more of the top ten killer diseases.

Pop science tells us that this disease is genetic. In the face of these statistics, we find that difficult to accept. After 150 generations of recorded history, it is doubtful that our gene pool collapsed in the last three generations. This is so, even after we allow for the environmental contamination by bioactive hormone like chemicals. Such an explanation ignores historical fact about this disease.

Today, thanks to endless contrived controversy and misleading advertisements, we are so poorly informed that we believe anything we are told. If a collapse of the gene pool is not responsible for this explosion, then what is responsible? The National Diabetes Information Clearinghouse classifies diabetes into three categories. They are: Type I diabetes, Type II diabetes and Other.

Type I diabetes accounts for l0% of the diabetes in the population today. "Other" is a catchall classification that includes perhaps 2% of the diabetes cases in the population. Type II diabetes accounts for roughly 88% of all cases drawn from the blood sugar control system failure mode caused by Hyperinsulinemia. The term "adult onset" is no longer appropriate because123,000 people under 20 years of age now have the disease.

As has been discussed hyperinsulinemia occurs when the cells in the body become insulin resistant. The body responds by increasing insulin in order to maintain blood sugar control. In the early stages it is able to successfully control blood sugar and most of the damage is done by the excess insulin that it takes to accomplish this. Later the insulin resistance becomes so severe that even with excess insulin blood sugar control is lost.

During the time that excess insulin characterizes the disease several other effects manifest. There are elevated triglyceride levels, arterial damage and atherosderosis. The arterial damage initially done by excess insulin in the blood stream activates the body’s repair mechanisms to repair the damaged blood vessels. This causes an elevation of lipoprotein-a, the repair protein, and a whole cascade of molecular and cellular swat team type responses to the apparent emergency.

The result is that the system deposits plaque in the arteries in an uncontrolled manner. If the circumstance is chronic, as is Hyperinsulinemia, the deposition of plaque continues until the artery becomes sufficiently occluded that it fails to supply adequate nutrients to its dependent organs. It is at this point that a heart attack or a stroke occurs.

Elevated levels of insulin reduce the high density lipids, HDL, the "good fats" in our blood stream. These lipids are responsible for removing excess cholesterol from the blood stream and transporting it to the liver where it is recycled. Less HDL means less cholesterol is removed. The liver, meanwhile continues to manufacture cholesterol regardless of whether we eat it in our diet or not.

It manufacturers approximately 85% of the total circulating cholesterol. With some of the HDL removed, the now relatively greater density of low density lipids, LDL, continue to transport it from the liver to the sites where it is needed. A resulting decrease in the HDL/LDL ratio and increase in the overall triglyceride density can now be observed.

As we have already shown, excess sugar in the system gets turned into long and medium chain saturated fat stored in our adipose cells. Through a metabolic process, some of this fat is converted into medium chain unsaturated fats which proceed to do oxidation damage to our arterial walls.

The processed foods that contain this excess sugar do not contain the antioxidants needed to neutralize this arterial damage. Overeating, particularly of processed foods, requires us to supplement the missing antioxidants to avoid this oxidative damage.

This is one of the two sources of unnatural fats that we find in our diet. Natural fats, even when they are unsaturated fats, are normally accompanied by the antioxidants that are required for their neutralization. This relationship is destroyed when we process our foods. The antioxidants that are normal to good food are removed.
Most of our fats and oils are not natural products; they are engineered products.

These products are engineered for sales appeal, shelf life, ease of manufacture and profit margin. Whenever they are re-engineered, one or more of these four product engineering targets dominates all of the engineering decisions. Nutrient value is, apparently, not a serious consideration in this process.

In the process of extracting, refining, bottling and distributing these fats and oils, the following operations are performed upon the raw seeds from which fats and oils are derived: Those components of the oils which spoil readily are removed.
These include fiber, protein, vitamins, essential amino acids, essential fatty acids, much of the minerals, lecithin, phytosterols, as well as a host of trace ingredients vital to health. High temperature and/or solvent methods are used to extract the oils from seeds. All grains are seeds. Flours of all types are processed with the same criterion. These two completely denatured foodstuffs are combined in your average dinner roll.

Oils are subjected to degumming, refining, bleaching, deodorizing and bottling. Some oils are also hydrogenated to produce other products, such as margarine. Seeds are a rich, concentrated source of many ingredients important to our health. Most, if not all, of them spoil and turn rancid at room temperatures quickly. The short shelf life of these nutrients, outside of the seed is what provokes producers to remove them.

Cholesterol is fat soluble. It does not dissolve in the blood stream which is mostly water. In order to be transported around in the blood, it must be carried by a lipoprotein carrier which has an affinity for water. When it is being carried from the liver to the rest of the body, the lipoprotein involved is LDL (low density lipoprotein). When cholesterol is being carried from the body back to the liver for recycling, the carrier is HDL (high density lipoprotein).

Thus LDL which distributes cholesterol throughout the body came to be known as the "bad" cholesterol and HDL which removes it from circulation came to be known as the "good" cholesterol. Hyperinsulinemia is characterized by a reduction in the HDL fraction and an increase in the LDL fraction. Clearly this sort of pop science that characterizes one essential lipoprotein as "good" and another as "bad" is the sort that comes from marketing and sales departments; certainly it does not originate in a reputable scientific laboratory.

Anyone interested in mitigating the disastrous effects of modern processed foods should limit sugar intake, entirely avoid hydrogenated fats and supplement a good source of unsaturated fats that contain the omega 3 essential fatty acids.
Although this is only the beginning in reversing a lifetime of damage, it is a start at extricating oneself from an unprecedented degenerative cycle. For more information on hyperinsulinemia get a complete copy of Insulin: Our Silent Killer, a well footnoted, eye opening report.

Most of the information in this article was culled from this report that fully documents the nature of diabetes. It describes the way the blood sugar control system works, identifies the role of insulin, defines the steps to a complete cure and describes the preventative precautions needed to stay disease free.

Insulin : Our silent Killer, A report on diabetes is  available through Valley Tech .Please call 970 669 9176 or write to Valley tech, Inc P.O.Box 7717 ,Loveland CO 80537 ,USA (www.healingmatters.com)