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 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.
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:
- 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.
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:
- 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.
- 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.
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 effects 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, vitamin A, 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 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.
Physical Signs and Symptoms of Diabetes
- 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.
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:
- 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.
- 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.
- 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.
- 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.
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:
- Interfering with absorption of essential minerals and creating deficiencies of the latter.
- Occupying a binding site on a metallo-enzyme, preventing the preferable mineral from attaching to that site and thus inhibiting vital enzymatic function.
- Altering the oxidation rate—resulting in either fast or slow oxidation.
- 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
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 antagonizes zinc and can replace zinc in vital metallo-enzyme binding sites.
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.
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 may act indirectly to produce symptoms of hypoglycemia, because mercury poisoning interferes with normal copper metabolism. See detoxification programs.
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:
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.
- Reduces gluconeogenesis, thus restoring glycogen reserves in the liver, which can be called upon to bolster blood sugar levels.
- 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.
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.
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.
- 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.
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.
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.
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.
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.
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.
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.
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.
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.
Copyright © 1987 - The Eck Institute of Applied Nutrition and Bioenergetics, Ltd.
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