Diabetes Mellitus

Description

Diabetes mellitus (DM) is a chronic disease in which there is an insufficiency of the hormone insulin or a resistance to the actions of insulin, or a combination of both.

Diabetes mellitus, perhaps more than any other disease, is strongly associated with Western culture and diet. DM is the most common of the serious metabolic diseases of humans. It is a chronic disorder of carbohydrate, fat and protein metabolism characterized by fasting hyperglycemia, glycosuria, and a greatly increased risk of atherosclerosis, microangiopathy, nephropathy and neuropathy.

The disease takes two primary forms:

Insulin-Dependent Diabetes Mellitus (IDDM, juvenile-onset, or Type 1) a ketosis-prone type of diabetes associated with histocompatibility antigens, beta-cell destruction and islet cell antibodies.

Non-Insulin Dependent Diabetes Mellitus (NIDDM, adult-onset, or Type 2) - a nonketosis-prone type of diabetes that is not secondary to other diseases. NIDDM has been subdivided into two subgroups: obese NIDDM and nonobese NIDDM.

Table 1 lists the typical characteristics of the two major clinical types of DM, Types 1 and 2.

Table 1. Characteristics of Diabetes Types 1 & 2
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Characteristic	IDDM	NIDDM
--------------------	------------------	--------------------
Age of onset	Typically <25	Typically >40
Body build	Lean	90% obese
Ketosis	Yes	No
Islet cell antibodies	Present at onset	Absent
HLA association	Positive	Negative
Family history	Minimal	Marked
Insulin secretion	Decreased	Normal or increased
Excessive urination & thirst	++	+
Weakness or fatigue	++	+
Excessive hunger with weight loss	++	-
Recurrent blurred vision	+	++
Vulvovaginitis or vulvar itching	+	++
Peripheral neuritis	+	++
Nighttime urination	++	-
Often asymptomatic	-	++
Predominant vascular disease	Microangiopathy	Atherosclerosis

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The incidence of DM in the United States is estimated at 4%, of which 90% are NIDDM and the rest IDDM. The prevalence of DM is rising and is now the seventh leading cause of death in the U.S. At the current rate of increase (6% per year) the number of diabetics will double every fifteen years.

Causes

Epidemiologically, DM has been linked to the Western lifestyle and is uncommon in cultures consuming a more "primitive" diet. As cultures switch from their native diets to the "foods of commerce" their rate of DM increases, eventually reaching the same proportions seen in Western societies.

Genetic Considerations
Extensive studies of identical and non-identical twins indicate genetic factors play an important role. In insulin-dependent diabetes, when one member of an identical twin had diabetes, there was a 20-50% chance the other did. In non-identical twins, there was only a 5% chance. In non-insulin-dependent diabetes, when one member of an identical twin had diabetes, there was an almost 100% chance the other had it. In contrast, there was only a 10% chance the non-identical twin had it.

Diet and Lifestyle
Although genetics appear important in susceptibility to diabetes, environmental factors are important in its induction. Many have been identified. A diet high in refined, fiber-depleted carbohydrate is believed to be diabetogenic in susceptible individuals, while a high intake of high-fiber, complex carbohydrate-rich foods is protective.

Obesity is another significant environmental factor, particularly considering the fact 90% of NIDDM types are obese. Even in normal individuals, significant weight gain results in carbohydrate intolerance, higher insulin levels, and insulin insensitivity in fat and muscle tissue. The progressive development of insulin insensitivity is believed to be the underlying factor in the genesis of NIDDM. Weight loss corrects all of these abnormalities and either significantly improves the metabolic disturbances of DM or converts overt diabetes into subclinical diabetes.

Insulin Dependent Diabetes Mellitus
IDDM is generally acknowledged to be due to an insulin deficiency. Although the exact cause is unknown, current theory suggests it is due to an hereditary pancreatic beta-cell predisposition to injury coupled with some defect in tissue regeneration capacity. Causes of injury are most likely hydroxyl and other free radicals, viral infection and autoimmune reactions.

Nitrosamines
Alloxan, a chemical used to induce experimental diabetes in animals, is a potent beta-cell toxin, causing destruction via free-radical formation. The N-nitroso derivative of glucosamine, has now replaced alloxan as the preferred agent for destruction of beta-cells in the induction of experimental diabetes. Circumstantial epidemiologic evidence suggests dietary intake of the N-nitroso-compounds found in smoked/cured meats is diabetogenic in susceptible individuals, producing beta-cell damage by the same mechanism as streptozocin. Many other chemicals, such as the rodenticide Vacor, have also been implicated in beta-cell damage.

Viral Infection
Recent epidemiological and experimental evidence has strengthened the hypothesis of a viral cause of IDDM in some cases. A viral cause was first suspected due to the seasonal variation in the onset of the disease (October to March). During these months, viral diseases, such as mumps, hepatitis, infectious mononucleosis, congenital rubella and coxsackie virus infections are much more prevalent. Viruses are capable of infecting pancreatic beta-cells and inducing DM.

Autoimmunity
Autoimmune factors may also be etiological in many cases. Antibodies to pancreatic cells (all types) are present in 75% of all cases of IDDM compared to 0.5 to 2.0% of normals. The antibody levels decline progressively after the first few weeks of the disease, suggesting beta-cell destruction and depletion of antigenic stimulus. It is probable the antibodies to the islet cells develop in response to cell destruction due to other mechanisms (chemical, viral, etc.) when normally concealed cellular antigens are exposed. It appears that normal individuals either do not develop as severe an antibody reaction, or are more able to repair the damage once it occurs.

Non-insulin Dependent Diabetes Mellitus
Central to the pathogenesis of NIDDM is insulin insensitivity as evidenced by typically high levels of circulating insulin and the reversibility of hyperglycemia by dietary changes and/or weight loss sufficient to restore insulin sensitivity.

Chromium
Considerable experimental and epidemiological evidence now indicates chromium levels are a major determinant of insulin sensitivity.

Chromium, an essential micronutrient, functions as a cofactor in all insulin-regulating activities. Its deficiency is wide spread in the U.S. For more discussion, see Nutritional Supplements.

Obesity
One importance of obesity in the etiology of diabetes is without dispute.

Obesity is associated with insulin insensitivity, and adipose size and distribution also seem to be important.

Weight loss, in particular a significant decrease in body fat percentage, is a prime objective in treating the majority of NIDDM patients since it improves all aspects of diabetes and may result in "cure."

Prenatal Factors
Recent epidemiological evidence has begun to support the concept prenatal malnutrition, in particular hyperglycemia, may be a promoter of DM, both types 1 and 2, later in life. Studies done in Berlin have shown adults born during the "hypocaloric war and post-war period (1941-48)" have significantly less DM that those born during the relatively hypercaloric years before and after. This is not a minor correlation, the data show a greater than 50% drop in the incidence of DM!

Another study shows a significantly lower incidence of childhood diabetes during periods in which maternal hyperglycemia was carefully controlled and the fetus protected from hyperinsulinism. Although the data in this study are based on a number of suppositions, they again indicate a greater than 50% drop in the incidence of childhood DM.

Signs & Symptoms

Both types
Excessive urination
Excessive thirst
Recurrent blurred vision
Fatigue

Juvenile onset
Bed-wetting
Weight loss

Adult onset
Usually asymptomatic, disease develops slowly
Vaginal yeast infections
Weight gain

Nutrient Depletion

Diabetic medications can rob the body of important nutrients, including:

Chromium This mineral is essential in the body’s metabolism of glucose. Chromium, in depleted levels, will not allow insulin to bind to receptor sites, preventing the clearance of sugar from the blood. Findings show that people with high insulin levels are likely to have low chromium levels, important as a consideration for individuals in the first stages of maturity-onset diabetes. When diabetics supplement chromium, both sugar and insulin levels decrease.

Magnesium Studies have demonstrated a relationship between magnesium deficiency and insulin resistance. An American Diabetes Association panel concluded that magnesium may play a role in insulin resistance and carbohydrate intolerance. Low dietary intake of magnesium may produce irritability, nervousness and less than optimal levels of neuromuscular control.

The incidence of hypomagnesemia is 25% to 39% among patients with diabetes.

Vitamin B 6 Studies have shown that B-6 supplementation may help repair eye problems associated with diabetes. Low levels of B-6 might create headaches, dizziness, numbness and irritability.

Diabetic medications may also affect the levels of manganese.

References:

Ellis, J. M., et al: A deficiency of vitamin B6 is a plausible molecular basis of the retinopathy of patients with diabetes mellitus, Biochem. Biophys. Res. Commun., Vol. 179, No. 1, 1991, pp. 615-619.

Mahan, K. & Escott-Stump, S: Krause's Food, Nutrition and Diet Therapy. Saunders, 1996.

Schnack, C.H.: Hypomagnesemia in Type II (Non-Insulin-Dependent) Diabetes Mellitus., Diabetologia, 1992;35:904-905.

Tinker-LF; Heins-JM; Holler-HJ. Commentary and translation: 1994 nutrition recommendations for diabetes. Diabetes Care and Education, a Practice Group of the American Dietetic Association [see comments] J-Am-Diet-Assoc. 1994 May; 94(5): 507-11.

Nutritional Supplements

Dietary Considerations

Dietary modification and treatment is fundamental to the successful treatment of DM. The incidence of DM is highly correlated with the fiber-depleted, high-refined carbohydrate diet of "civilized" man.

Reestablishing a healthy diet and lifestyle reverses the carbohydrate and lipid metabolism abnormalities associated with the "foods of commerce" and eventually results in a low prevalence of DM. The epidemiological evidence indicting the Western diet and lifestyle as the ultimate etiological factor in DM is overwhelming.

Clinical trials of dietary treatment with a more primitive diet, high in plant cell-wall materials and complex carbohydrates and low in fat and animal products, have consistently demonstrated superior therapeutic effects over oral hypoglycemic agents, insulin (when less than 30 units per day), and other previously recommended dietary regimes (carbohydrate restriction, high protein and the ADA diet).

The high-carbohydrate, high plant-fiber (HCF) diet popularized by James Anderson has substantial support and validation in the scientific literature as the diet of choice in the treatment of DM. It is high in cereal grains, legumes and root vegetables and restricts simple sugar and fat intake. The caloric intake consists of 70-75% complex carbohydrates, 15-20% protein and only 5-10% fat, and the total fiber content is almost 100 grams per day. The positive metabolic effects of the HCF diet are many: reduced post-meal hyperglycemia and delayed hypoglycemia, increased tissue sensitivity to insulin, reduced cholesterol (but increased HDL) and triglyceride levels, and progressive weight reduction. If patients resume a conventional diet, their insulin requirements return to prior levels.

On the HCF diet, available carbohydrate calories come from grain products (50%), fruits and vegetables (48%) and skim milk (2%). Protein is provided by fruits and vegetables (50%), grain products (36%), and skim milk and lean meat (14%). The fat is derived form grain products (60%), fruits and vegetables (20%), and skim milk and meat (12%). The HCF diet is also based on the exchange system with more information and dietary guidelines available from the HCF Diabetes Research Foundation (1872 Blairmore Rd, Lexington, Ky 40502). A representative menu for the maintenance HCF diet is shown in Table 2.

Table 2. Representative Menus for the HCF and MHCF Diets
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HCF Diet                         MHCF Diet

Breakfast

whole oats, 1 c	oat bran cereal, 1 c
whole wheat bread, 2 sl	yogurt, plain low fat, 1 c
skim milk, 1c	blueberries, 1/2 c
grapefruit, 1/2
margarine, 2 pats

Snack (morning or afternoon)

yogurt, 1/2 c	apple, 1 medium
fresh strawberries, 1 c	whole grain flat bread
	cracker, 2

Lunch

whole wheat bread, 2 sl	brown rice, cooked, 1/2 c
kidney bean and rice casserole, 1 c	lentil soup, 1/2 c
kale, cooked, 1 c	carrot, 1 large
cucumber & onion salad	celery, 1/2 large
potatoes, boiled, 1/2 c	onion, 1/4 cup
garlic, 1 clove
margarine, 4 pats

Dinner

whole wheat bread, 2 sl	whole grain bread, 1 sl
lima beans, 1/2 c peas, 3/4 c	green beans, 3/4 c
blackberries, 3/4 c	tossed salad, 2 c
tomato, 1 small	broccoli, 3/4 c
asparagus, steamed, 1/4 c	salmon, 4 oz
squash, winter, 1 c	butter, 1 pat
beef, roast, 4 oz
margarine, 4 pats

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IDDM patients have also benefited from the HCF diet. In one representative study, when 16 IDDM patients were treated with HCF diets, their average insulin requirements dropped by 38% and they demonstrated significantly lower fasting, postprandial and urinary glucose levels than matched patients on control diets.

Modified High Fiber Content Diet (MHCF): In general, the HCF Diet and/or the Low Fat Diet (Pritikin) are adequate for the treatment of diabetes mellitus. However, improvements can be made, primarily by substituting more natural (i.e., primitive) foods wherever possible in the HCF Diet and avoiding some foods that have deleterious effects. The MHCF Diet is higher in leguminous fibers than any of the other diets, limits processed grains and excludes fruit juices, low fiber fruits, skim milk and margarine.

There is substantial rationale for these modifications. Legumes are low in fat and high in complex carbohydrates and fiber and are proven effective in treating DM. Fruit juices, low fiber juices and processed grains (i.e., flour) induce a rapid elevation of serum glucose and insulin levels, and the casein in skim milk appears to raise cholesterol levels. The trans-fatty acids in margarine (and other synthetically saturated fats) also have significant injurious effects.

A comparison of the ADA (American Diabetes Association), HCF and MHCF diets is shown in Table 3. A typical menu plan for the MHCF Diet is presented in Table 2.

Table 3. Composition of the ADA, HCF and MHCF
Diets (all values in grams except ratios)
===========================================

	ADA	HCF	MHCF
Protein	98	96	90
Carbohydrate	215	351	370
Simple (S)	100	94	70
Complex (C)	115	257	300
S/C ratio	0.87	0.3	0.23
Fat	83	23.5	20
Saturated (S)	19	4.7	4.0
Monounsaturated (M)	43	9.5	7
Polyunsaturated (P)	15	6.9	8
P/S ratio	0.79	1.47	2.0
Cholesterol	0.47	0.04	0.05
Fiber	27	82	100
Soluble (S)	15	67	80
Insoluble (I)	12	15	20
S/I ratio	1.25	4.47	5.0

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Dietary Fiber, Guar and Pectin
Supplementation with the plant fibers guar (5 g/meal) and pectin (10 g/meal) has demonstrated a positive impact on diabetic control. These fiber supplements are now being used, along with the standard ADA diet, by many diabetologists. Jenkins and colleagues developed a palatable crisp bread containing guar gum. When diabetic patients ate between 14 and 26 grams of guar per day they required less insulin and had less glycosuria. It is interesting to note that these beneficial effects are maximal in patients on a diet containing at least 40% complex carbohydrates.

Legumes
Consumption of legumes should be encouraged since a high carbohydrate, legume-rich, high-fiber diet has been shown to improve all aspects of diabetic control. The beneficial effects of legumes are primarily due to their water-soluble, gel-forming fiber components which have effects similar to those of guar and pectin.

Fiber Supplementation vs. High Fiber Diet
Although fiber-supplemented diets are beneficial, they are not as effective as the HCF diet and are therefore reserved for the NIDDM patient who is unwilling to implement the more difficult dietary change and will settle for palliative results. Insulin dosages on fiber supplemented diets can usually be reduced to one-third those used on control (ADA) diets, while the HCF diet has led to discontinuation of insulin therapy in approximately 60% of NIDDM patients, and significantly reduces doses in the other 40% .

Sucrose
Sugar is actually an anti-nutrient for diabetics. Sucrose must be eliminated as its consumption produces elevated plasma cholesterol, triglyceride, and uric acid levels; diminished glucose tolerance; increased platelet adhesiveness; and a change in platelet electrophoretic behavior, all of which are associated with diabetes and atherogenesis.

Exercise
An appropriate exercise training program is vitally important in a DM treatment plan. It improves many parameters and is indicated in both IDDM and NIDDM. Physically trained diabetics experience many benefits: enhanced insulin sensitivity with a consequent diminished need for exogenous insulin, improved glucose tolerance, reduced total serum cholesterol and triglycerides with increased HDL levels that result in a more anti-atherogenic state and, in obese diabetics, improved weight loss.

However, a physical fitness program does present some risk to the diabetic and must be carefully adapted to the fitness of the patient. Exercise should be avoided during periods of hypoglycemia. Besides its well-known and documented value, exercise may have a more specific beneficial effect for diabetics: exercise increases tissue levels of chromium (in rats) and increases the number of insulin receptors in IDDM patients. It is possible, then, that many of the beneficial effects of exercise are directly related to improved chromium metabolism.

Homeopathic Remedy

1.*Uranium nitrate tinct.	begin with 12X - 30C if needed
2. Arsenicum bromatum	30X or tincture (4 drops x day in water)
3. Helonias Dioica tinct.	6C to 30C
4. Rhus aromatica	6X
5. Uranium nitrate tinct.	30C
6. Arsenicum bromatum	30C
7. Aceticum acidum	30C

Treatment Schedule

Doses cited are to be administered on a 3X daily schedule, unless otherwise indicated. Dose usually continued for 2 weeks. Liquid preparations usually use 8-10 drops per dose. Solid preps are usually 3 pellets per dose. Children use 1/2 dose.

Legend

X = 1 to 10 dilution - weak (triturition)
C = 1 to 100 dilution - weak (potency)
M = 1 to 1 million dilution (very strong)
X or C underlined means it is most useful potency

Asterisk (*) = Primary remedy. Means most necessary remedy. There may be more than one remedy - if so, use all of them.


References

Boericke, D.E., 1988. Homeopathic Materia Medica.

Coulter, C.R., 1986. Portraits of Homeopathic Medicines.

Kent, J.T., 1989. Repertory of the Homeopathic Materia Medica.

Koehler, G., 1989. Handbook of Homeopathy.

Shingale, J.N., 1992. Bedside Prescriber.

Smith, Trevor, 1989. Homeopathic Medicine.

Ullman, Dana, 1991. The One Minute (or so) Healer.

Herbal Approaches

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Herbs
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Bilberry
Common garlic plant / Allium sativum
Fenugreek seeds
Gymnema sylvestre
Momordica charantia (Bitter melon)
Onion plant (Allium cepa)
Pterocarpus marsupium

Note: The misdirected use of an herb can produce severely adverse effects, especially in combination with prescription drugs. This Herbal information is for educational purposes and is not intended as a replacement for medical advice.

Discussion:

Since antiquity, diabetes mellitus has been treated with plant extracts. Recent scientific investigation has confirmed the efficacy of many of these preparations, some of which are remarkably effective. This discussion will, of necessity, be limited to a few plants, those which appear most effective, are relatively nontoxic, and have substantial documentation of efficacy.

Allium cepa and Allium sativum

The bulbs of the common onion plant and common garlic plant, have significant oral hypoglycemic action. Experimental and clinical evidence suggests onions and garlic lower glucose levels by competing with insulin for insulin-inactivating compounds, resulting in an increase of free insulin.

The forms and quantity of onion and garlic in the diet are sufficient to have significant physiological effects. Graded doses of onion extracts (1 ml of extract = 1 g of whole onion) at levels sometimes found in the diet, i.e., 25 to 200 grams, reduce blood sugar levels during oral and intravenous glucose tolerance tests and adrenaline-induced hyperglycemia in a dose-dependent manner. The anti-hyperglycemic effects are similar in both raw and boiled onion extracts.

The cardiovascular effects of garlic and onions, i.e., lipid lowering, platelet aggregation inhibition, antihypertensive, etc., further substantiate the liberal use of these common foods by the diabetic patient.

A decoction of the leaves of the blueberry has a long history of folk use in the treatment of DM. Oral administration reduces hyperglycemia in normal and depancreatized dogs even when glucose is concurrently injected intravenously.

The glycoside myrtillin is apparently the most active ingredient. Upon injection it is somewhat weaker than insulin, but is less toxic, even at 50 times the 1 g/d therapeutic dose. It is of great interest to note a single dose can produce beneficial effects lasting for several weeks.

Fenugreek seeds have demonstrated anti-diabetic effects in experimental and clinical studies. The active principle is in the defatted portion of the seed which contains the alkaloid trogonelline, nicotinic acid and coumarin. It is believed that chronic intake of fenugreek seeds produces a vagal hypersensitization as evidenced by increased pancreatic peptide (PP) release.

Administration of the defatted seed (in daily doses of 1.5-2 g/kg) to both normal and diabetic dogs reduces fasting and postprandial blood levels of glucose, glucagon, somatostatin, insulin, total cholesterol and triglycerides, while increasing HDL-cholesterol and PP levels. Studies have not yet determined whether these effects are due to the known components, an unknown compound, or the high fiber content of the seeds.

Jerusalem artichokes have a favorable influence on blood glucose. (Rumessen , 1990)

Momordica charantia (or Bitter melon, also known as balsam pear) is a tropical vegetable widely cultivated in Asia, Africa and South America, and has been used extensively in folk medicine as a remedy for DM. The hypoglycemic action of the fresh juice, aqueous extract or dried extract of the unripe fruit has been clearly established in both experimental and clinical studies. Momordica charantia is composed of several compounds with confirmed anti-diabetic properties.

Charantin, extracted by alcohol, is a hypoglycemic agent composed of mixed steroids. Oral administration to rabbits of 50 mg/kg reduces blood sugar 42%. In other animal studies it has been found that this hypoglycemic action is reduced, but not eliminated, in animals whose pancreases have been removed, suggesting pancreatic as well as extrapancreatic mechanisms.

Momordica also contains an insulin-like polypeptide, polypeptide- P, which lowers blood sugar levels when injected subcutaneously into IDDM patients. Since it appears to have fewer side effects than insulin, it has been suggested as a replacement for some patients.

The insulin secretagogue activity of both the whole plant and some of its extracts have been confirmed in vitro, and oral administration of 50-60 ml of the juice has shown good results in clinical trials.

Pterocarpus marsupium has a long history of use in India as an indigenous treatment for diabetes. The flavonoid, (-)- epicatechin, extracted from the bark of this plant, has been shown to prevent alloxan-induced beta-cell damage in rats.

Further, both epicatechin and a crude alcohol extract of Pterocarpus marsupium have been shown to actually regenerate functional pancreatic beta-cells. No other drug or natural agent has been shown to generate this activity.

Another recent import from India is Gymnema sylvestre, which has been used for diabetes for 2,000 years. Data suggest that Gymnema regenerates and repairs the islets of Langerhans (where insulin is produced) and enhances the release of insulin in diabetic subjects.

The common name for Gymnema is "Gurmar" (meaning sugar destroyer) and it does seem to prevent the absorption and activity of glucose molecules. It does not represent a cure for diabetes but can help significantly in keeping glucose levels within acceptable limits.

Milk thistle (Silybum) may also be used, especially when there is a co-morbid condition involving the liver, to even out insulin production and assist with insulin sensitivity.

The herbal sweetener of choice is Stevia.

Newall has compiled extensive lists of both hyperglycemic and hypoglycemic herbs. It is essential to be aware of all of these herbs in order to avoid negative interactions.

Hypoglycemic

Herb	Effect
Alfalfa	Hypoglycemic, manganese, human
Aloes/ Aloe vera	Hypoglycemic, in vivo
Burdock	Hypoglycenmic, in vivo
Celery	Hypoglycemic, in vivo
Cornsilk	Hypoglycemic, in vivo
Damiana	Hypoglycemic
Elecampane	Hypoglycemic
Eucalyptus	Hypoglycemic, in vivo
Fenugreek	Hypoglycemic, human
Garlic Plant	Hypoglycemic, in vivo, human
Ginger	Hypoglycemic, in vivo
Ginseng, Panax	Hypoglycemic
Juniper	Hypoglycemic in vivo
Marshmallow	Hypoglycemic
Myrrh	Hypoglycemic
Nettle	Hypoglycemic
Sage	Hypoglycemic, in vivo
Tansy	Hypoglycemic, in vivo

Hyperglycemic

Herb	Effect
Devil's Claw	Contra-indicated in diabetics
Elecampane	Hyperglycaemic
Figwort	Contra-indicated in diabetics (like Devil's Claw)
Ginseng, Panax	Hyperglycemic
Gotu Kola	Hyperglycaemic, human
Licorice	Reduced K aggravates glucose tolerance

References:

Akhtar, MS et al., Effect of momordica charantia on blood glucose level of normal and aloxan-diabetic rabbits. Planta Med. 1981, 42:205-212.

Keder, P & Chakrabarti, C: Effects of bittergourd (Momordica charantia) seed and glibenclamide in streptozocin-induced diabetes mellitus. Ind. J. Exp. Biol. 1982, 20:232-235.

Newall CA, Anderson LA, Phillipson JD. Herbal Medicines: A Guide for Health-care Professionals. London: The Pharmaceutical Press, 1996.

Ribes, G et al., Effects of fenugreek seeds on endocrine pancreatic secretions in dogs. Ann. Nutr. Metab. 1984:28.

Rumessen J.J., et al. Fructans of Jerusalem artichokes: Intestinal transport, absorption, fermentation, and influence on blood glucose, insulin, and C-peptide responses in healthy subjects. Am J Clin. Nutri 52 (1990): 675-68 I.

Velussi, M et al., Silymarin reduces hyperinsulinemia, malondialdehyde levels and daily insulin need in cirrhotic diabetic patients. Curr. Ther. Res. 1993, 53(5):533-545.

Vuorinen-Markkola, H et al., Guar gum and insulin-dependent diabetes: effects on glycemic control and serum lipoproteins. The Am. J. Clin. Nutr. 1992, 56:1,056-1,060.

Walji, H: Diabetes: a modern health crisis. Natural Health Series, Kian Press, 1997.

Aromatherapy - Essential Oils

Eucalyptus Essence,	Geranium Essence,
Juniper Essence,	Onion Essence.

Related Health Conditions

Atherosclerosis
Cataract
Coronary heart disease
Eye disorders
Fatigue
Glaucoma
Hypoglycemia
Insufficient blood circulation
Kidney disease
Obesity
Vaginitis
Yeast infection

Drug Interactions

Diabetics are extremely vulnerable to any dietary excesses, or shortcomings. Unfortunately, responses are often erratic, making calculations of insulin dosages extremely tricky.

Drugs (chiefly insulin pharmaceutical) can also impact appetite, taste and gastrointestinal functions. Specifically, so far as nutritional status is concerned:

High insulin levels seem to be related to low chromium levels.

Insulin resistance is often associated with magnesium deficiency.

Diabetics record only half the manganese levels of the normal populaiton.

Diabetics tend to excrete large amounts of zinc.

Glucose tolerance improves when supplements of vitamin B 6 are taken.

Abstracts

References

Abdel-Aziz, M.T., Abdou, M.S., Soliman, K., et al: Effect of carnitine on blood lipid patterns in diabetic patients. Nutr Rep Int 29:1071-9, 1984.

Akhtar, M.S., Athar, M.A., & Yaqub M. Effect of momordica charantia on blood glucose level of normal and alloxan-diabetic rabbits. Planta Medica 42:205-12, 1981.

Allen, F.M. Blueberry leaf extract: Physiologic and clinical properties in relation to carbohydrate metabolism. JAMA 89:1577-81, 1927.

Anderson, J.W. & Ward, K. High-carbohydrate, high-fiber diets for insulin-treated men with diabetes mellitus. Am J Clin Nutr 32:2312-21, 1979.

Anderson, J.W. High polysaccharide diet studies in patients with diabetes and vascular disease. Cereal Foods World 22:12-22, 1977.

Anonymous: Translation of the diabetes nutrition recommendations for health care institutions. American Diabetes Association. Diabetes Care, 20:106-8, 1997 Jan.

Anonymous: Translation of the diabetes nutrition recommendations for health care institutions: position statement. American Diabetes Association [comment]. J Am Diet Assoc, 97:52-3, 1997 Jan.

Anonymous: Role of fat replacers in diabetes medical nutrition therapy. American Diabetes Association [comment]. Diabetes Care, 19:1302-3, 1996 Nov.

Baghurst, K., Raj, M., & Truswell, A. Onions and platelet aggregation. Lancet 1:101. 1977.

Bever, B.O. & Zahnd, G.R. Plants with oral hypoglycemic action. Quart J Crude Drug Res 17:139-96. 1979.

Blair SN et al., Physical activity, nutrition, and chronic disease. Med Sci Sports Exerc, 28:335-49, 1996 Mar.

Boden, G. et al: Effects of vanadyl sulfate on carbohydrate and lipid metabvolism in patients with NIDDM. Metab. Clin. Exp. 1996, 45(9): 1,130-1,135.

Boland E & Savoye M: Nutrition strategies for adolescents with insulin-dependent diabetes mellitus. Lippincotts Prim Care Pract, 1:341-7, 1997 Jul-Aug.

Brownlee, M., Vlassara, H., & Cerami, A. Nonenzymatic glycosylation and the pathogenesis of diabetic complications. Ann Int Med 101:527-37, 1984.

Burkitt, D. & Trowell, H. Western Diseases: Their Emergence and Prevention. Harvard Univ Press, Cambridge, MA.

Casassus P, Fontbonne A, Thibult N, et al. Upper-body fat distribution: a hyperinsulinemia-independent predictor of coronary heart disease mortality. Arterioscler Throm 1992;1387-92.

Ceriello, A., Giugliano, D., Russo, P.D., & Passariello, N. Hypomagnesemia in relation to diabetic retinopathy. Diabetes Care 5:558-9, 1982.

Chakravarthy, B.K., Gupa, S., Grambhir, S.S. Gode KD: 1-Epicatechin a novel anti-diabetic drug. Indian Drugs 18:184-5, 1981.

Chakravarthy, B.K., Gupa, S., & Gode, K.D. Antidiabetic effect of (-)-epicatechin. Lancet 2:272, 1982.

Chakravarthy, B.K., Gupa, S., Gambhir, S.S., & Gode, K.D. Pancreatic beta-cell regeneration in rats by (-)-epicatechin. Lancet 2:759-60, 1981.

Chaudhry, P.S., Cambrera, J., Juliani, H.R., & Varma, S.D. Inhibition of human lens aldose reductase by flavonoids, sulindac and indomethacin. Biochem Pharmacol 32:1995-8, 1983.

Chen, K. Understanding and treatment of diabetes mellitus by Traditional Chinese Medicine. Am J Clin Med. 9 (1) (1981): 93-94.

Coggeshall, J.C., Heggers, J.P., Robson, M.C., & Baker, H. Biotin status and plama glucose in diabetics. Ann NY Acad Sci 447:389-92, 1985.

Crane MG, Sample C. Regression of diabetic neuropathy with total vegetarian (vegan) diet. J Nutr Med 1994;4:431-9.

Cunningham, J. et al: Vitamin C: An Aldose Reductase Inhibitor. Journal of the American College of Nutrition, 1993;12(5):617 /Abstract 129.

Davidson, S. The use of vitamin B12 in the treatment of diabetic neuropathy. J Flor Med Assoc 15:717-20, 1954.

Dolhofer, R. & Wieland, O. Increased glycosylation of serum albumin in diabetes mellitus. Diabetes 24:417-22, 1980.

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