The release of insulin is
facilitated by calcium and inhibited by magnesium.
Thus the proper ratio of calcium to magnesium is critical for
optimal insulin secretion.
Chromium acts synergistically with insulin.
Chromium — Insulin Relationship
Chromium deficiency is widespread in the United States, due
to excessive sugar and carbohydrate intake and to soil depletion.
Chromium definitely acts as a synergist with insulin. Research by
Mertz (1969), indicates at least five possibilities:
Insights Into the
Causes, Mechanisms and Correction of Hypoglycemia, Dysinsulinism and
Diabetes
By Dr. Paul C. Eck
and
Dr. Larry Wilson

2225 W. Alice Avenue - Phoenix, Arizona 85021 USA 1-602-995-1580
This material is for educational purposes only
The preceding statements have not been evaluated by the
Food and Drug Administration
This information is not intended to diagnose, treat, cure or prevent any
disease.
Copyright © 1987 - The Eck Institute of Applied Nutrition and
Bioenergetics, Ltd.
Introduction
Diabetes, hypoglycemia and dysinsulinism are three of the
most common metabolic dysfunctions afflicting Americans today. It has been
estimated that there are well over three million diagnosed diabetics and at
least three times as many more that remain undiagnosed. At least 50 percent of
our population suffers from the symptoms of hypoglycemia to some extent.
Diabetes is now a leading cause of blindness and kidney
disease. Hypoglycemia is recognized as an important cause of fatigue,
alcoholism, crime, hyperkinetic behavior, learning disabilities, behavioral
disorders, anxiety, depression, allergies and many other physical, mental and
emotional problems.
The use of hair analysis and the New Nutrition concepts allow
for a much deeper understanding of the causes, identification and correction of
these common conditions.
The Mechanism Of Blood Sugar Utilization
Before discussing the various dysfunctions associated with
deviations in blood sugar metabolism, it will be helpful to review the mechanism
of glucose regulation in the body.
Storage And Release Of Glucose
Ingested sugars and carbohydrates are absorbed as simple
sugars and pass to the liver, where some sugar is allowed to enter the general
circulation. However, the majority of ingested glucose is normally converted to
glycogen, the storage form of sugar and is stored mainly in the liver.
Any reduction in the circulating blood sugar levels normally
stimulates glucocorticoid hormone production by the adrenal glands. One effect
of increased cortisone output is to cause the liver to reconvert glycogen into
glucose and release it into the blood. In this way, optimum blood sugar levels
are normally maintained.
Dysfunction of the adrenal glands, either a deficiency of
adequate hormone production or, an excess, seriously interferes with normal
blood sugar regulation.
Optimal adrenal function requires the presence of certain
nutrients such as manganese, zinc, vitamin C, pantothenic acid and vitamin E. In
addition, the adrenal hormones are synthesized from cholesterol, so that a
deficiency in the synthesis of cholesterol will impair adrenal function.
Adrenal gland activity is also a function of the metabolic or
oxidation rate, which is in turn, is governed by the nutritional balance and by
the activity of the sympathetic nervous system.
Insulin Metabolism
Insulin is a polypeptide hormone, which is necessary for the
utilization of glucose in the body. The function of insulin allows glucose to
pass through the cell membrane.
The presence of excess sugar in the blood stimulates the
release of insulin from the beta cells in the Islets of Langerhans of the
pancreas. Zinc is closely involved with insulin synthesis, secretion and
function.
Zinc — Insulin Relationship
Zinc has a complicated relationship to insulin. Research
reveals the following:
| • |
At the pH of the pancreas, insulin can only be crystallized in the presence of zinc, cadmium, cobalt and nickel ions. |
| • |
Crystalline insulin is coated with zinc, the more zinc that can be made to adhere to the insulin molecule, the longer the duration of insulin's action. |
| • |
There is evidence that zinc is utilized in the beta cells of the pancreas to both store and release insulin as required. Release of insulin from the beta cells is accompanied by a loss of zinc. |
| • |
Zinc seems to have a similar action to insulin, in stimulating uptake of glucose by adipose tissue. A deficiency of zinc results in reduced uptake of glucose by adipose tissue. |
| • |
Injection of Dithiazone, a zinc chelating agent, produces diabetes in experimental animals. |
| • |
Pancreatic tissue of diabetic individuals has been shown to have one-third the zinc concentration of controls. |
| • |
Zinc may be necessary for retention of chromium, which plays a vital role in glucose metabolism. |
| • | Chromium could stabilize the structure of the insulin molecule in its most effective form. |
| • | Chromium may inhibit tissue insulinase. Insulinase terminates the biological activity of insulin. |
| • | Chromium could increase the binding of insulin to the tissues. |
| • | Chromium could be a co-factor for a cell membrane transfer mechanism of insulin. |
| • | Chromium could facilitate the initial reaction between insulin and a specific cell membrane receptor site. |
Chromium is utilized in the form of
Glucose Tolerance Factor, in which chromium is combined with four amino
acids.
A deficiency of chromium definitely results in impaired
insulin function, which may result in either a hypoglycemia syndrome or
diabetes.
Transport Of Nutrients Across Cell
Membranes
The transport of nutrients across the cell membrane is
regulated, in part, by the sodium pump mechanism, which regulates the
electrical potential and osmotic pressures across cell membranes. The
proper amount and balance between sodium and potassium in the cell
environment are therefore, also critical to the utilization of glucose.
The cell membrane permeability is also regulated by
calcium. Calcium acts as a stabilizer of cell membrane potential. Excess
calcium, for example, renders the cells less permeable to glucose as well as
to insulin.
Metabolism Of Glucose Within The Cells
Once inside the cells, the combustion or utilization of
glucose depends on the availability of enzyme co-factors and activators.
Among the most important of these is magnesium, which is a vital
component of numerous intra-cellular enzymes and manganese, vitamins B1,
B2, B3 and B6, which are required for the glycolysis cycle, the first
part of the energy-producing mechanism. Iron, copper, magnesium, B1 and
B2 are required as co-factors and activators of the Krebs cycle and the
electron transport system, which completes the burning of glucose, to
produce energy in the form of adenosine-triphosphate (ATP).
Blockage, due to a deficiency of any of the above nutrients,
at any step of this process, will result in symptoms of diabetes or
hypoglycemia, depending on at exactly what step in the energy cycle that the
blockage occurs.
Thyroid hormone also plays a vital role, in as much as
thyroxin regulates the rate of combustion of glucose within the cells.
Summary Of Causes Of Blood Sugar
Disturbances
The possible causes of diabetes and hypoglycemia can include
any combination of the following:
| • |
A deficiency of manganese, zinc, B-complex, vitamin C, or vitamin E; impaired adrenal function, affecting cortisone secretion, which in turn, affects glycogen release from the liver. |
| • |
Imbalanced oxidation rate affects glucocorticoid hormone release. |
| • |
Zinc deficiency prevents adequate production of insulin. |
| • |
A low calcium/magnesium ratio diminishes the release of insulin from the beta cells of the pancreas. |
| • |
A deficiency of chromium prevents proper transport and attachment of insulin to cell receptor sites. |
| • |
Imbalances in sodium, potassium, calcium and magnesium interfere with cell membrane function, preventing glucose and/or insulin from entering the cells. The body may then compensate by raising the sugar level to force sugar into the cells. |
| • |
A deficiency of enzyme co-factors in the Krebs and glycolysis cycles impairs glucose utilization. The body again may compensate for low energy production by raising blood sugar levels in an attempt to force more sugar into the cells. |
| • |
Abnormal thyroid activity affects the rate of sugar combustion within the cells. With this overview in mind, we will focus on each metabolic dysfunction condition in greater detail. |
Hypoglycemia
A Cellular Dysfunction
Hypoglycemia, simply stated, is defined as low blood sugar.
However, many individuals with normal or even high glucose tolerance tests
frequently manifest many of the symptoms of low blood sugar.
This occurs because there is confusion about the definition
and meaning of hypoglycemia. While the word hypoglycemia strictly
refers to low glucose in the blood, many individuals use the term loosely to
designate a specific group of symptoms arising from inadequate glucose
metabolism. Inadequate glucose metabolism can have many causes, one of which
is a decreased availability of glucose in the blood. Other causes
include: 1) low levels of glucose in the cells (cellular hypoglycemia) and
2) adequate levels of glucose in the cells, but inadequate combustion of
that glucose.
To help dispel the confusion, in this article hypoglycemia
refers to the syndrome of inadequate glucose utilization by the cells, for
any reason.
The reason for defining hypoglycemia as a cellular problem,
is that it is within the cells that glucose is utilized.
Using this definition, it becomes obvious that the use of a
blood test for hypoglycemia is not always reliable. Many individuals who
have had a 5-hour glucose tolerance test are well aware of this inadequacy.
Their test report was normal, but they suffered all the symptoms of low
sugar during the test.
Diagnosis Of The Hypoglycemia Syndrome
If the blood serum test is not reliable, what indicators can
be used? Several simple questions are often a reflective indicator:
| 1) |
Ask the patient how he feels if he goes without eating more than about 4 hours. The hypoglycemic usually cannot do this without experiencing symptoms of fatigue, extreme hunger, weakness, irritability, or mental confusion. |
| 2) |
Ask how he feels after he ingests sugar or sweets, without balancing it with other types of foods such as fats or proteins. In some forms of hypoglycemia, eating sugar or simple carbohydrates will bring on distressing symptoms. Another screening tool used as an indicator is tissue mineral analysis. |
Hair Analysis
By studying thousands of cases of hypoglycemia, Dr. Paul Eck
discovered certain mineral patterns associated with this condition. These
are referred to as trends, because they indicate a tendency, but are
not diagnostic in and of themselves. These trends can only be read out on a
hair analysis performed without washing the hair and with proper laboratory
controls. Trends include:
| • |
Imbalance in the calcium/magnesium ratio, especially a ratio between 3.6/l and 4.5/l, or 8.5/1 and 9.7/1. |
| • |
Slow oxidation, especially with very low levels of potassium (below 5.0 mgs/%), or a very high calcium/potassium ratio (higher than 100/1 mgs./%). |
| • |
Fast oxidation, especially if it is extreme and/or accompanied by a low zinc level and imbalanced (high or low) calcium/magnesium ratio or a high sodium/potassium ratio. |
The following section explains the
rationale for these empirically observed trends.
Causes Of Hypoglycemia
Fast Oxidation and Excessive Gluconeogenesis
Fast oxidation refers to a mineral pattern of low tissue
calcium and magnesium levels relative to sodium and potassium levels.
Fast oxidation, with a high sodium/potassium ratio, is
associated with the alarm stage of stress, characterized by rapid
metabolism of food and over-activity of the thyroid and adrenal glands. True
fast oxidation is found in approximately 10% of the population and is
associated with one specific type of hypoglycemia.
The increased adrenal gland activity associated with fast
oxidation causes a state of continuous gluconeogenesis, or conversion of
glycogen to glucose. The end-result is a mild to severe depletion of liver
glycogen reserves.
Hyperactivity of the thyroid gland causes excessively fast
burning of glucose, which results in rapid depletion of liver glucose
reserves.
When additional extra glucose is suddenly required (usually
due to stress) and the glycogen reserves of the liver are depleted, the
result is the manifestation of acute symptoms of low blood sugar.
The fast oxidizer is prone to what is referred to as reactive
hypoglycemia, in which blood sugar levels, after a meal, rises dramatically
and then fall precipitously.
This type of hypoglycemia can readily be brought on by
certain foods or activities that speed up the oxidation rate. Sweets,
alcohol, coffee, overwork, exercise,or stress of any kind can readily
trigger acute symptoms of hypoglycemia in a fast oxidizer.
Various food supplements such as vitamin C, vitamin E and
B-complex may, because of their stimulatory affects on metabolism, produce
the same effect.
Hypoglycemia in the Slow Oxidizer; Inadequate Gluconeogenesis and
Impaired Membrane Transport
Slow oxidation is a condition indicated on a tissue mineral
analysis readout by high calcium and magnesium levels, relative to sodium
and potassium levels. Slow oxidation represents a state in which the thyroid
and adrenal glands are relatively under-active. Adrenal insufficiency
results in the production of less than normal amounts of glucocorticoid
hormones.
Faced with a need for an increase in blood sugar, the body
cannot secrete adequate levels of cortisone to stimulate sufficient
conversion of glucose from glycogen in the liver; the end result is
hypoglycemia.
The slow oxidizer has an additional problem that contributes
to the hypoglycemia syndrome; transport of glucose across the cell membranes
is impaired, due to low levels of sodium and potassium and an elevated
calcium level. Therefore, even if glucose levels in the blood are adequate,
glucose may not be transported in adequate amounts across the cell
membranes.
The slow oxidizers are the group of individuals who may
exhibit many of the symptoms of hypoglycemia, while reporting normal, or
near-normal, glucose levels on a 5-hour glucose tolerance test.
The slow oxidizer has a third problem that frequently may
result in symptoms associated with the hypoglycemia syndrome. In slow
oxidation, the burning of glucose within the cells is more or less
dysfunctional and inefficient.
Glucose may enter the cells, but is not metabolized
adequately, due to a deficiency of enzyme co-factors and/or diminished
thyroid hormone activity. These factors can initiate hypoglycemia symptoms,
even if glucose is available in the blood and is adequately transported into
the cells.
In the slow oxidizer, hypoglycemia symptoms are often
chronic. Symptoms include, chronic fatigue, a constant craving for sweets,
mental confusion and depression. Symptoms are frequently aggravated or
triggered by fatigue, which further reduces adrenal activity.
Hypoglycemic symptoms also may be triggered by eating certain foods, which
slow the oxidation rate such as; dairy foods, high fat diet, or a low
protein diet.
The use of calcium, magnesium and zinc supplements, vitaminA,
vitamin D and copper supplements may also aggravate hypoglycemic symptoms
inasmuch as these nutrients tend to lower the metabolic rate. Vigorous
exercise may temporarily alleviate hypoglycemic symptoms by temporarily
stimulating adrenal gland activity. However, in the long run, unless adrenal
activity is sufficiently restored, vigorous exercise can worsen hypoglycemia
associated with slow oxidation by causing increased exhaustion of the
adrenal glands.
Diabetes
Definition
Diabetes mellitus literally refers to sugar in the urine. As
with hypoglycemia, this term tells us nothing about the cause of this
increasingly common metabolic dysfunction. In more modern terms, diabetes
refers to a specific pattern of glucose tolerance, in which the blood sugar
level rises excessively and remains elevated for several hours, above the
normal glucose tolerance curve.
Diabetes is often viewed as a simple deficiency of insulin.
Nothing could be further from the truth. The concept that diabetes is due to
a deficiency of insulin is too simplistic and outdated.
Diabetes occurs with normal or even elevated insulin levels
and is due to a variety of causes and mechanisms.
Mechanisms Of Diabetes
Diabetes in the Fast Oxidizer
The fast oxidizer burns glucose too rapidly and therefore has
an increased demand for insulin. The fast oxidizer is also particularly
prone to a zinc deficiency, because zinc is lost as the body goes into the
alarm stage of stress, which characterizes fast oxidation.
A high insulin requirement and a tendency to a zinc
deficiency can combine in the fast oxidizer to produce a deficient insulin
type of diabetes. The deficiency of zinc is intimately associated with
insufficient production or diminished release of insulin.
Fast oxidizers are also characterized by a low calcium level.
Calcium, in optimal amounts, is required for the release of insulin and thus
another type of insulin deficiency diabetes results from a calcium
deficiency.
This type of diabetes is further accentuated when magnesium
levels are high relative to calcium levels, inasmuch as magnesium inhibits
insulin release.
Diabetes in the Slow Oxidizer
Slow oxidizers may also suffer from a zinc deficiency, or low
calcium to magnesium ratio, with the same consequences as the fast oxidizer.
However, other dysfunctions prevail in the slow oxidizer, which predisposes
one to diabetes.
Slow oxidation is characterized by impaired or blocked
transport of glucose across cell membranes and inadequate utilization of
glucose within the cells.
An elevated tissue calcium and magnesium level together with
a deficiency of sodium and potassium can result in an impairment of cell
membrane permeability. In such situations, the body may raise blood sugar
levels to help force sugar into the cells. In these cases, insulin levels
are normal or even high,the body may raise insulin levels to help force
glucose into the cells.
Glucose passing into the cells fails to be metabolized
properly in the glycolysis cycle in slow oxidation. Failure of sufficient
glucose to be transported across the cell membrane may be due to a
deficiency of manganese, bio-unavailable magnesium, toxic metals, deficiency
of B vitamins or decreased thyroid hormone activity. The body may attempt to
compensate for a reduction of energy production, again by raising blood
sugar and insulin levels.
Slow oxidizers are usually deficient in manganese and
frequently deficient in chromium and zinc as well. While the zinc level may
appear to be normal, zinc is low relative to copper if the
zinc/copper ratio is less than 5/1. Calcium/magnesium and sodium/potassium
ratio imbalances can also occur in the slow as well as the fast oxidizer.
Diabetes And Hypoglycemia Syndrome Can
Coexist
A common misconception is that a person is either
hypoglycemic or diabetic. The fact is, one of the major symptoms of diabetes
is extreme fatigue and diabetics generally suffer from cellular
hypoglycemia. The reasons for this are:
| • |
Since insulin is necessary for glucose absorption into the cells, a deficiency of insulin blocks adequate glucose from entering the cells, resulting in a cellular hypoglycemia syndrome. |
| • |
Some cases of diabetes result from or are aggravated by a chromium deficiency, which impairs attachment of insulin to cell membrane receptor sites. The end result is an impairment of glucose transport into the cells, resulting in low cellular glucose levels. |
| • |
Some cases of diabetes are due to an excess bio-unavailability of tissue calcium, which impairs the transport of glucose across the cell membranes. The body raises blood glucose levels in these cases, to help force glucose into the cells. In these cases also, there can be a cellular hypoglycemia, in spite of excess glucose in the blood. |
| • |
Some cases of diabetes are associated with, or are aggravated by, a manganese deficiency. In these cases, adequate levels of insulin may be released, but not transported in sufficient amounts to receptor sites on the cell membrane. Again, this causes inadequate glucose absorption into cells and cellular hypoglycemia results. |
| • |
A deficiency of manganese also inhibits the activity of the enzyme pyruvate carboxylase, which is necessary for sugar and carbohydrate metabolism in the glycolysis cycle. Even if adequate glucose reaches the cells, energy production from the glucose is inadequate, leading to symptoms of hypoglycemia. |
| • |
Slow-oxidizer diabetes is associated with inadequate thyroid function. A deficiency of adequate cellular thyroid hormones causes slow burning of glucose, even if glucose is readily available. |
Recognition Of Diabetes
Early recognition of diabetes is vitally important because
diabetes is a primary cause of so many other metabolic dysfunctions,
including kidney disease, atherosclerosis, blindness and diabetic
neuropathy.
A simple finger stick blood test, or a single urine
evaluation is clearly inadequate, because sugar levels fluctuate greatly
with diet and physical activity.
The 5-hour glucose tolerance test is the standard diagnostic
test for diabetes. However by the time this test is performed, a person may
have had diabetes for several years and damage of vital organs and numerous
other metabolic dysfunctions may have begun.
This problem can be largely avoided if early signs and
symptoms of diabetes are recognized.
| • |
Skin tags - These are millimeter sized flaps of skin that appear in warm areas of the body, such as armpits or under the breasts. Skin tabs have a blood supply and can drop off as rapidly as they appear, without leaving a scar. |
| • |
Extreme exhaustion not related to activity. As glucose levels increase, energy levels often fall off drastically. Periods of utter exhaustion occur from out of the blue. Fatigue can occur suddenly, without any warning. |
| • |
Loss of Libido - Related to glucose related zinc deficiency. |
| • |
Frequent urination - Glucose acts as an osmotic diuretic, taking water with it as it is eliminated in the urine. |
| • |
Excessive thirst, due to a loss of water from excessive urination. |
| • |
Burning sensation on urination. |
| • |
Thickened toenails, with fibrous material underneath. |
| • |
Discoloration of the toenails. Nails first turn yellow, then brownish as the condition worsens. |
| • |
Increased curvature of the nails and tendency for ingrown toenails. |
| • |
Toenails may actually fall off from the base in some cases. |
| • |
Encrustation of the eyelashes. At times, the eyes are glued shut in the morning and pus may exude from the eyes, particularly upon awakening. |
| 1) |
A low sodium to potassium ratio (less than 1.5/1). This ratio is intimately associated with excessive protein catabolism and glucocorticoid secretion. In diabetics, glucose cannot be oxidized in sufficient amounts to be converted to energy-rich adenosine-triphosphate (ATP). As a result, the body is forced to convert protein to glucose to maintain energy production. |
| 2) |
A high or low calcium to magnesium ratio (greater than 10/1 or less than 3.3/1), especially when combined with a low sodium to potassium ratio. Since calcium and magnesium are involved in insulin release, an imbalance in this mineral ratio is indicative of blood sugar dysfunction. |
| 3) |
Low chromium, zinc and/or manganese levels, especially when combined with the previously listed trends. As explained earlier, each of these minerals is intimately involved in insulin function and carbohydrate metabolism. |
| 4) |
Elevated iron (above 5.0 mgs./%), or copper (above 3.5 mgs./%) levels, especially when combined with a low sodium to potassium ratio. An elevated iron level is an excellent indicator of excessive tissue protein catabolism. Iron is being released due to excessive breakdown of tissue cells. Iron, by being also antagonistic to chromium, can cause a chromium deficiency. Excess copper antagonizes zinc and is associated with protein catabolism as well. |
Diabetic Trends Derived
From A Hair Analysis
Indicators of diabetes from a hair analysis represent another
valuable way of early detection of diabetes. The most important mineral
trends are:
Tissue mineral analysis can be
utilized as an excellent screening tool. If a person has one or more of the
above trends and exhibits some of the physical symptoms listed above, it
would be prudent to check urine or blood sugar levels.
The more mineral trends and/or symptoms, the more likely a
blood sugar intolerance is present. For instance, a low chromium level,
together or coupled with a sodium/potassium inversion, indicates diabetes
more than either of these indicators alone.
One particular advantage of tissue mineral analysis
methodology is that we can begin correction of the mineral imbalances, even
before the glucose tolerance test reveals a problem.
The Role Of Toxic Metals In Hypoglycemia
And Diabetes
Toxic metals can directly or indirectly play a role in the
causation of both diabetes and hypoglycemia. A toxic metal may precipitate
blood sugar dyscrasia by:
| 1) |
Interfering with absorption of essential minerals and creating deficiencies of the latter. |
| 2) |
Occupying a binding site on a metallo-enzyme, preventing the preferable mineral from attaching to that site and thus inhibiting vital enzymatic function. |
| 3) |
Altering the oxidation rate — resulting in either fast or slow oxidation. |
| 4) |
Forcing another type of compensation or adaptation to the stress generated by the toxic metal, resulting in an alteration of a critical ratio, such as the calcium/magnesium or sodium/potassium ratio. These mineral ratio imbalances then cause a blood sugar dysfunction. |
Specific Toxic Metals
Associated With Hypoglycemia And Diabetes
Iron
One specific diabetic pattern is associated with elevated
tissue iron levels. The most probable mechanism in high-iron diabetes is
that iron may cause a chromium deficiency thereby hindering the utilization
of insulin. Iron is also antagonistic with manganese and it is possible that
this is a factor as well.
Cadmium
Cadmium antagonizes zinc and can replace zinc in vital
metallo-enzyme binding sites.
Copper
Copper antagonizes zinc, raises calcium and slows oxidation
by impairing adrenal and thyroid function. Many slow oxidizers with
hypoglycemic symptoms can be traced to an elevated copper level.
Calcium
We have mentioned that excess tissue calcium levels interfere
with cell membrane permeability and may be responsible for inadequate
transport of glucose into body cells.
Mercury
Mercury may act indirectly to produce symptoms of
hypoglycemia, because mercury poisoning interferes with normal copper
metabolism.
Dysinsulinism
Definition
The term dysinsulinism refers to a glucose tolerance curve
that exhibits characteristics of both hypoglycemia and diabetes.
Dysinsulinism is considered a transition stage between the two, in which
there may be alternating symptoms of both hypoglycemia and diabetes.
According to Dr.Eck's research, dysinsulinism is associated with a
calcium/magnesium ratio between 3.3/1 and 3.6/1 or between 9.8/1 and 10.0/1.
Correction Of Diabetes, Hypoglycemia And Dysinsulinism
| Correction Of
Hypoglycemia In The Fast Oxidizer Correction requires slowing the oxidation rate: |
||
| • | Reducing excessive corticosteroid output accomplishes two purposes: | |
| 1) |
Reduces gluconeogenesis, thus restoring glycogen reserves in the liver, which can be called upon to bolster blood sugar levels. |
|
| 2) |
Restores a reserve of corticosteroid hormones. The combination of more available cortisone and more available glycogen allows adrenal cortisone output to be increased upon demand and ensures a reserve of glycogen to be drawn upon when necessary. |
|
| • |
Reducing excessive thyroid activity helps slow the excessive rate of glucose metabolism in the fast oxidizer, thereby reducing the possibility of depletion of glucose reserves. |
|
| • |
Raising low calcium levels and reducing excessively high potassium and sodium levels, slows transport of glucose and thyroid hormone into the cells, which also contributes to slowing the combustion of glucose. |
|
Diet
A diet high in fat, particularly animal fats, tends to slow
the excessive oxidation rate. There may be several mechanisms for this:
| • |
Fats are digested and absorbed slowly from the intestine. Therefore, fats do not exert a stimulatory effect on metabolism the way rapidly absorbed sugars do. |
| • |
Fat consumption also enhances absorption of the fat-soluble vitamins A and D. Vitamin A acts synergistically with zinc to lower sodium levels, slowing the oxidation rate and vitamin D increases calcium absorption from the gut, also tending to slow the oxidation rate, by reducing excessive glucocorticoid activity. |
| • |
Fast oxidizers tend to have difficulty with that part of the energy production cycle known as the Krebs cycle. Fats provide a high level of acetates, which play an essential role in this part of the energy production system. |
| • |
Fat is also a high-energy food as compared to either carbohydrates and proteins, yielding 9 calories per gram. Fast oxidizers benefit from this higher energy fuel. |
| Low Carbohydrates and Sugars | |
| • |
Carbohydrate foods frequently contain phytates, which lower calcium, magnesium and zinc levels. Calcium, magnesium and zinc are required to slow an excessive oxidation rate, so a low carbohydrate diet tends to spare these essential nutrients. |
| • |
Sugars and carbohydrates are more rapidly absorbed and have a more stimulatory effect on metabolism. |
| Supplementary Nutrients | |
| • |
Nutrients such as calcium, zinc magnesium, copper, vitamin A, D, B2, B12, choline and inositol are also helpful to slow an excessive oxidation rate. |
|
Correction Of Hypoglycemia In The Slow Oxidizer The solution for these individuals is to reactivate adrenal and thyroid activity. |
|
| • |
Increased secretion of adrenal cortical hormones allows release and conversion of more glycogen to glucose from liver storage sites, thus improving blood sugar levels. |
| • |
Increased adrenal function raises sodium and potassium levels, which improves transport of glucose into cells. |
| • |
Increase in thyroid hormones promotes more efficient combustion of glucose within the cells. |
| • |
Improved adrenal hormone reserves permit increased secretion of cortisone, when glucose demands increase suddenly — as occurs during stress, or during prolonged exercise. |
Diet
A diet high in the low-fat proteins, adequate in complex
carbohydrates and low in fat tends to speedup the rate of metabolism.
Carbohydrate is relatively rapidly absorbed and phytates as
contained in grains favor faster oxidation. Protein in the diet stimulates
glandular function, raises sodium and lowers magnesium, thus favoring fast
oxidation.
Dietary fat slows the rate of metabolism and is therefore
ideally kept to a minimum.
Supplementary Nutrients
Vitamin A, vitamin C, vitamin E, the B-complex (particularly
vitamin B1) and manganese specifically enhance adrenal function. Manganese,
the B-complex and vitamin E enhance thyroid and intracellular glucose
metabolism.
Zinc is particularly essential for protein metabolism and is
frequently deficient in the slow oxidizer, in part due to an elevated copper
level.
Potassium is required and recommended to help lower
excessively high calcium levels, thus improving thyroid function and
transport of nutrients across the cell membranes.
Frequently, toxic metals are present such as cadmium, copper,
mercury and nickel. These toxic metals block various enzyme functions and
must be slowly removed by giving appropriate mineral antagonists, oral
chelating agents and by balancing the oxidation rate.
Correction Of Diabetes In The Fast
Oxidizer
Correction requires improving insulin secretion, transport
and utilization.
Raising low calcium, zinc, chromium and manganese levels
serve to improve insulin synthesis, secretion and transport.
Slowing the oxidation rate reduces excessive adrenal cortical
hormone production, which reduces conversion of glycogen to glucose and
contributes to lowering of blood sugar levels.
Diet
The same general dietary recommendations apply for the fast
oxidizer diabetic as for the fast-oxidizer hypoglycemic.
Fat has a sparing action on insulin, because fat slows the
emptying time of the stomach, causing slower absorption of sugars into the
blood.
Reducing the quantity of starches and sugars in the diet
reduces the influx of sugars into the blood from the intestine and hence
reduces insulin requirements.
Supplementary Nutrients
Fast-oxidizer type diabetics benefit from calcium, both
because it slows the rate of oxidation, thus sparing insulin and because
calcium promotes the release of insulin from the beta-islet cells of the
pancreas.
Additional zinc and chromium are added to all diabetics'
programs, two tablets of each twice a day, because of the importance of
these minerals in insulin production and utilization.
Frequently, diabetes in the fast oxidizer is associated with
elevated iron levels and/or elevated cadmium levels. If this is the case,
specific nutrients may be given as indicated to reduce elevated iron and
cadmium levels. Copper, manganese and chromium, in excess, interfere with
iron absorption. Calcium, selenium, vitamin C, copper and zinc may be given
as indicated to reduce excessive cadmium levels.
Correction Of Diabetes In The Slow
Oxidizer
The slow-oxidizer diabetic should follow the same general
dietary guidelines as have been described for the slow-oxidizer
hypoglycemic.
Since the cause of slow-oxidizer diabetes has more to do with
inadequate transport of glucose into the cells and inadequate insulin
utilization, rather than inadequate production of insulin, different
measures are indicated.
Diet
Restriction of simple sugars is less critical in the
slow-oxidizer diabetic than in the fast oxidizer. However, refined sugars
should definitely be avoided as they lack the essential mineral elements.
Fats should be avoided inasmuch as they slow down the
metabolic rate further.
Low-fat proteins tend to improve the metabolic rate by
stimulating adrenal and liver function. Phytates contained in grains assist
in lowering excessively high calcium levels.
Supplementary Nutrients
Potassium and sodium-raisers (nutrients which serve to
increase sodium levels) are recommended to reduce elevated tissue calcium
levels because high tissue calcium levels interfere with both insulin
secretion and glucose transport across cell membranes. Sodium and potassium
levels must also be increased to improve functioning of the sodium-potassium
pump mechanism.
The above measures help glucose to enter body cells. If
glucose can be made more available to the cells, the compensation of an
elevated blood sugar will no longer be necessary.
Manganese is a critical element for the slow oxidizer
individual; not only because it is involved in insulin transport, but
because it raises one's sodium level. This in turn, enhances the transport
of glucose into the cells and improves both adrenal and thyroid activity.
Thyroid hormone speeds up the rate of burning of glucose within the cells.
Even if transport across the cell membrane is adequate,
glucose may build up within the cells, if it is not adequately metabolized.
B-complex vitamins and vitamin E are also required to enhance
thyroid activity.
Chromium and zinc are also recommended for the slow-oxidizer
diabetic in the dose of one tablet of each, twice a day. An elevated copper
level in the slow oxidizer often interferes with zinc metabolism. Chromium
levels tend to be borderline-low in all oxidation types.
Adrenal and thyroid protomorphogens support glandular
function and assist in increasing a slow oxidation rate.
Prevention Of Hypoglycemia And Diabetes
The same principles of nutrient deficiencies, toxic metals
and biochemical imbalances, can be applied to a person to prevent as well as
to treat hypoglycemia and diabetes. Prevention is really the wiser choice.
It is far less costly and less time-consuming than treating a full-blown
case of illness.
Undoubtedly, eating a high-quality diet that contains
adequate manganese, zinc, chromium, copper and other essential nutrients are
one simple way of prevention. However, today even our natural foods are
deficient in these vital elements, due to agricultural methods, storage and
processing methods. Good diet alone is not sufficient assurance against the
development of hypoglycemia and diabetes.
Hair analysis provides a simple, relatively inexpensive,
early screening test in which the trends for illness can be recognized;
often several years before symptoms become manifest. Also, the test provides
us with direction for action to correct the nutrient imbalances that are
currently present, to avoid more advanced pathology.
The Correction Process — The Time Factor
The correction process for both hypoglycemia and diabetes
depends on many factors. Requiring in rare instances as little as several
months, but more likely requiring up to several years, depending upon which
nutrients are deficient and how severe the mineral ratio imbalances. There
is, at present, no way to tell how long will be required from a single hair
analysis, or from symptoms alone.
Cranton and Passwater in their book, Nutrition, Trace
Elements and Hair Analysis, state that it requires 2 years to restore to
normal, low chromium levels. In some individuals, it is also necessary to
restore manganese, zinc and numerous other nutrients, as well as chromium.
The elimination of toxic metals must also be slow and
unforced. Rapid removal of toxic metals tends to upset body chemistry,
because the toxic metals frequently serve an adaptive and supportive
function. The body will seldom allow their releases until vital mineral
reserves have been built-up sufficiently and the body chemistry is stable
enough to withstand the release of toxic crutches.
Retracing
During the correction process, a diabetic may pass through a
stage of hypoglycemia. This occurs because hypoglycemia is an earlier stage
of metabolic dysfunction and as the mineral patterns return toward normal,
the body may temporarily pass back through a phase of hypoglycemic mineral
ratios and levels. This ordinarily is no cause for alarm and regular
retesting will minimize any possible symptoms.
It is also possible to pass through another diabetic pattern
during the correction process. This also is temporary and due to the complex
changes in the mineral balance that occur as toxic metals are removed and
essential minerals act to compensate and adapt to the changes taking place
in the body chemistry.
Energy levels will also vary during the recovery process.
Since both diabetic and hypoglycemic individuals suffer from a periodic
energy loss, they may become dismayed if, after a period of improvement, an
energy loss later occurs. Again, this is no cause for alarm. Energy loss may
occur on the program at any point, due to:
| • |
Use of energy within the body for restoring vital body functions, causing diminished availability of energy for external activity. |
| • |
Rebalancing of the body chemistry, causing a temporary slowdown in metabolism. Occasionally, metabolism may speed up greatly, also resulting in a temporary energy loss. |
| • |
Change in another mineral level or ratio which is intimately related to energy production, such as a change in iron, copper, manganese, sodium, or calcium balance. |
Conclusion
Both hypoglycemia syndrome and diabetes are complex
biochemical dysfunctions, whose causes are multiple in nature. We have
attempted to present the underlying pathophysiology of these metabolic
dysfunctions, as well as to explain the principles of a new nutritional
approach to their correction.
Through the use of tissue mineral analysis and application of
the principles of the mineral balancing approach to correction of body
chemistry; we have had excellent success in both preventing and reversing
many of the signs and symptoms of these common conditions.

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