Text Size

Site Search powered by Ajax

Diabetes Mellitus

Diabetes Mellitus


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

Characteristic IDDM NIDDM
-------------------- --------------------------------------
Age of onsetTypically <25Typically >40
Body buildLean90% obese
Islet cell antibodiesPresent at onsetAbsent
HLA associationPositiveNegative
Family historyMinimalMarked
Insulin secretionDecreasedNormal 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 diseaseMicroangiopathyAtherosclerosis

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.


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.

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.

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.

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.

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

Juvenile onset
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.


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
HCF Diet                         MHCF Diet


whole oats, 1 coat bran cereal, 1 c
whole wheat bread, 2 slyogurt, plain low fat, 1 c
skim milk, 1cblueberries, 1/2 c
grapefruit, 1/2
margarine, 2 pats

Snack (morning or afternoon)

yogurt, 1/2 capple, 1 medium
fresh strawberries, 1 cwhole grain flat bread
cracker, 2


whole wheat bread, 2 slbrown rice, cooked, 1/2 c
kidney bean and rice casserole, 1 clentil soup, 1/2 c
kale, cooked, 1 ccarrot, 1 large
cucumber & onion saladcelery, 1/2 large
potatoes, boiled, 1/2 conion, 1/4 cup
garlic, 1 clove
margarine, 4 pats


whole wheat bread, 2 slwhole grain bread, 1 sl
lima beans, 1/2 c peas, 3/4 cgreen beans, 3/4 c
blackberries, 3/4 ctossed salad, 2 c
tomato, 1 smallbroccoli, 3/4 c
asparagus, steamed, 1/4 csalmon, 4 oz
squash, winter, 1 cbutter, 1 pat
beef, roast, 4 oz
margarine, 4 pats


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)

Simple (S)1009470
Complex (C)115257300
S/C ratio0.870.30.23
Saturated (S)194.74.0
Monounsaturated (M)439.57
Polyunsaturated (P)156.98
P/S ratio0.791.472.0
Soluble (S)156780
Insoluble (I)121520
S/I ratio1.254.475.0


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.

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% .

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.

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 bromatum30X or tincture (4 drops x day in water)
3. Helonias Dioica tinct.6C to 30C
4. Rhus aromatica6X
5. Uranium nitrate tinct.30C
6. Arsenicum bromatum30C
7. Aceticum acidum30C

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.


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.


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


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.


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.


AlfalfaHypoglycemic, manganese, human
Aloes/ Aloe vera Hypoglycemic, in vivo
BurdockHypoglycenmic, in vivo
CeleryHypoglycemic, in vivo
CornsilkHypoglycemic, in vivo
EucalyptusHypoglycemic, in vivo
FenugreekHypoglycemic, human
Garlic PlantHypoglycemic, in vivo, human
GingerHypoglycemic, in vivo
Ginseng, PanaxHypoglycemic
JuniperHypoglycemic in vivo
SageHypoglycemic, in vivo
TansyHypoglycemic, in vivo


Devil's ClawContra-indicated in diabetics
FigwortContra-indicated in diabetics (like Devil's Claw)
Ginseng, PanaxHyperglycemic
Gotu KolaHyperglycaemic, human
LicoriceReduced K aggravates glucose tolerance


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

Coronary heart disease
Eye disorders
Insufficient blood circulation
Kidney disease
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.



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.

Dosch, H-M.: The Possible Link Between Insulin Dependent (Juvenile) Diabetes Mellitus and Dietary Cow Milk, Clinical Biochemistry, 1993;26:307-308.

Drash, A. L.: Nutrition and the Etiology of Insulin-Dependent Diabetes Mellitus. Nutrition & the MD, February, 1993;19(2):1-3.

Drner, G., Mohnike, A., & Thoelke, H. Further evidence for the dependence of diabetes prevalence on nutrition in perinatal life. Exp Clin Endocrinol 84:129-33, 1984.

Drner, G., Steindel, E., Thoelke, H., & Schliack, V. Evidence for decreasing prevalence of diabetes mellitus in childhood apparently produced by prevention of hyperinsulinism in the foetus and newborn. Exp Clin Endocrinol 84:134-42, 1984. Ed: Manganese and glucose tolerance. Nutr Rev 26:207-10, 1968.

Editorial: Low-Level Nitrates May Promote Diabetes. Medical Tribune, December 24, 1992;24/Diabetes Care, 1992;15:1505-1507.

Editorial: New recommendations and principles for diabetes management. Nutr-Rev. 1994 Jul; 52(7): 238-41.

Editorial: Nutrition recommendations and principles for people with diabetes mellitus. Diabetes-Care. 1994 May; 17(5): 519-22.

Editorial: Nutrition recommendations and principles for people with diabetes mellitus [see comments] J-Am-Diet-Assoc. 1994 May; 94(5): 504-6.

Ellis, J. M., Folkers, K., Minadeo, M., VanBuskirk, R., Xia, Li-Jun, Tamagawa, H., 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.

Facchini F, Chen Y-DI, Reaven GM. Light-to-moderate alcohol intake is associated with enhanced insulin sensitivity. Diabetes Care 1994;17:115.

Fagen, C. et al: Nutrition management in women with gestational diabetes mellitus: a review by ADA's Diabetes Care and Eduication dietetic practice group.. J.A.D.A. 1995 April; 95(4): 460-467.

Faure, P. et al: Lipid Peroxidation and Trace Element Status in Diabetic Ketotic Patients: Influence of Insulin Therapy., Clinical Chemistry, 1993;39(5):789-793.

Gapparov MM: [Sugar substitutes in specialized child nutrition products for the prevention and treatment of diabetes mellitus]. Vopr Pitan, :68-70, 1996.

Gerstein H. Cow milk exposure and type I diabetes mellitus. Diabetes Care 1994;17:13-9.

Goodman, L. & A. Gilman. 1975. The Pharmacological Basis of Therapeutics. Macmillan, New York.

Green A: Nutrition and environmental factors in insulin-dependent diabetes
mellitus: a genetic-epidemiological perspective. Proc Nutr Soc, 56:225-31, 1997 Mar.

Groop, P-H. et al: Long-Term Effects of Guar Gum in Subjects with Non-Insulin-Dependent Diabetes Mellitus, American Journal of Clinical Nutrition, 1993;58:513-518.

Gunderson EP: Intensive nutrition therapy for gestational diabetes. Rationale and current issues. Diabetes Care, 20:221-6, 1997 Feb.

Helgason, T. & Johasson, M.R. Evidence for a food additive as a cause of ketosis-prone diabetes. Lancet 2:716-20, 1981.

Helman A: Nutrition and general practice: an Australian perspective. Am J Clin Nutr, 65:1939S-1942S, 1997 Jun.

Henry RR, Gumbiner B. Benefits and limitations of very-low-calorie diet therapy in obese NIDDM. Diabetes Care 1991;14:802-23.

Hersey III WC, Graves JE, Pollack ML, et al. Endurance exercise training improves body composition and plasma insulin responses in 70- to 79-year-old men and women. Metabol 1994;43:847-54.

Hughes, J.H. & A.L. Latner. Chlorophyll and Hemoglobin Regeneration after Hemorrhage. Journal of Physiology, 86. 1936.

Isida K, Mizuno A, Murakami T, Shima K. Obesity is necessary but not sufficient for the development of diabetes mellitus. Metabolism 1996;45:1288-95.

Jain, S.R., Sharma, S.N. Hypoglycaemic drugs of Indian indigenous origin. Planta Med. 15: 439-442, 1967.

Jain, S. C. et al: A Study of Response Pattern of Non-Insulin Dependent Diabetes to Yoga Therapy., Diabetes Research and Clinical Practice, 1993;19:69-74.

Jenkins, D.J.A., Wolever, T.M.S., Bacon, S., et al: Diabetic diets: High carbohydrate combined with high fiber. AM J Clin Nutr 33:1729-33, 1980.

Jones, C.L. & Gonzales, V. Pyridoxine deficiency: A new factor in diabetic retinopathy. J Am Pod Assoc 68:646-53, 1978.

Karter AJ, Mayer-Davis EJ, Selby JV, et al. Insulin sensitivity and abdominal obesity in African-American, Hispanic, and non-Hispanic white men and women. Diabetes 1996;45:1547-55.

Kay, R., Grobin, W., & Trace, N. Diets rich in natural fiber improve carbohydrate tolerance in maturity onset, noninsulin dependent diabetics. Diabetologia 20:12-23, 1981.

Keder, P. & Chakrabarti, C. Effects of bittergourd (Momordica charantia) seed and glibenclamide in streptozotocin induced diabetes mellitus. Ind J Exp Biol 20:232-5, 1982.

Kiechl S, Willeit J, Poewe W, et al. Insulin sensitivity and regular alcohol consumption: large, prospective, cross sectional population study Bruneck study. BMJ 1996;313:1040-4.

Kirschmann, J.D. 1990. Nutrition Almanac: Nutrition Search. McGrew-Hill: New York.

Koivisto, V.A. & DeFronzo, R.A. Exercise in the treatment of type II diabetes. Acta Endocrin suppl 262:107-111, 1984.

Koivisto, V.A. & Yki-Jarvinen, H.: Fructose and Insulin Sensitivity in Patients With Type II Diabetes. Journal of Internal Medicine, 1993;233:145-153.

Krotkiewski, Bjrntorp, Sjostrom & Smith. Impact of obesity on metabolism in men and women. J CLin Invest 72:1150-62, 1983.

Krumdiek, C.L. 1976. Folic Acid. Present Knowledge In Nutrition, 4th ed. The Nutrition Foundation, New York, Washington.

References L - P

Lam, S., Harfenist, E., Packham, M., et al: Investigation of the possible mechanisms of pyridoxal 5'-phosphate inhibition of platelet reactions. Thrombosis Res 20:633-45, 1980.

Landin K, Holm G, Tengborn L, Smith U. Guar gum improves insulin sensitivity, blood lipids, blood pressure, and fibrinolysis in healthy men. Am J Clin Nutr 1992;56:1061-5.

Landoifi, R. Modification of platelet bioflavonoids: Structure - activity relation. Biochem Pharmacol 33:1525-30, 1984.

Lardinois, C. K.: The Role of Omega-3 Fatty Acids on Insulin Secretion and Insulin Sensitivity. Medical Hypotheses, 1987;24:243-248.

Law CM: Fetal and infant influences on non-insulin-dependent diabetes mellitus (NIDDM). Diabet Med, 13:S49-52, 1996 Sep.

Lehmann T et al., Nutritional recommendations for diabetic patients: adaptation of the recommendations defined by the Diabetes and Nutrition Study Group of EASD. Schweiz Rundsch Med Prax, 85:1570-3, 1996 Dec 3.

Levine, R., Streeten, D., & Doisy, R. Effect of oral chromium supplementation on the glucose tolerance of elderly human subjects. Metabolism 17:114-25, 1968.

Long SD, Swanson MS, O’Brien K, et al. Weight loss in severely obese subjects prevents the progression of impaired glucose tolerance to type II diabetes. Diabetes Care 1994;17:372

Lubin, B. & Machlin, L. Biological aspects of vitamin E. Ann NY Acad Sci 393:, 1982.

Mahabir D & Gulliford MC: Use of medicinal plants for diabetes in Trinidad and Tobago. Rev Panam Salud Publica, 1997 Mar, 1:3, 174-9.

Makino, K. et al: Plasma Lipoprotein (a) Levels in Patients Having Chronic Renal Failure With and Without Diabetes Mellitus., Atherosclerosis, 1993;98:255-256.

Mann, G.V. Hypothesis: The role of vitamin C in diabetic angiopathy. Perspect Biol Med 17:210-7, 1974.

Mann JI: The role of nutritional modifications in the prevention of macrovascular complications of diabetes. Diabetes, 1997 Sep, 46 Suppl 2:, S125-30.

Marshall, J. A. et al: The Role of Dietary Fiber and the Etiology of Non-Insulin-Dependent Diabetes Mellitus: The San Luis Valley Diabetes Study. Annals of Epidemiology, January 1993;3(1):18-26.

Matz-R: Parallels between treated uncontrolled diabetes and the refeeding syndrome with emphasis on fluid and electrolyte abnormalities. Diabetes-Care. 1994 Oct; 17(10): 1209-13.

McCann, V.J. & Davis, R.E. Serum pyridoxal concentrations in patients with diabetic retinopathy. Aust N Z J Med 8:259-61, 1978.

Merck. The Merck Index: An Encyclopedia Of Chemicals And Drugs. 9th edition, Rahway, N.J.: Merck & Co., 1976.

Miller, J. et al: Rice: A High or Low Glycemic Index Food? American Journal of Clinical Nutrition, 1992;56:1034-36.

Murray, M.T., & J.E. Pizzorno. 1991. Encyclopedia of Natural Medicine. Rocklin, Ca; Prima Publishing.

Norwell, D. & Tarr, R. Garlic, Vampires and CHD. Osteo Ann 12:276-80, 1984.

Offenbach, E. & Pistunyer, F. Beneficial effect of chromium-rich yeast on glucose tolerance and blood lipids in elderly patients. Diabetes 29:919-25, 1980.

Oliver-Bever, B., Zahnd, G.R.: Plants with oral hypoglycaemic action. Quart. J Crude Drug Res. 17: 139-196, 1979.

Osterode W et al., Nutritional antioxidants, red cell membrane fluidity and blood viscosity in type 1 (insulin dependent) diabetes mellitus. Diabet Med, 13:1044-50, 1996 Dec.

Paolisso, G. et al: Pharmacologic Doses of Vitamin E Improve Insulin Action in Healthy Subjects and in Non-Insulin-Dependent Diabetic Patients., American Journal of Clinical Nutrition, 1993;57:650-6.

Parillo, M., et al: A High-Monounsaturated-Fat/Low-Carbohydrate Diet Improves Peripheral Insulin Sensitivity in Non-Insulin-Dependent Diabetic Patients. Metabolism, December 1992;41(12):1373-1378.

Park KS, Hree BD, Lee K-U, et al. Intra-abdominal fat is associated with decreased insulin sensitivity in healthy young men. Metabol 1991;40:600-3.

Parker, D. R. et al: Relationship of Dietary Saturated Fatty Acids and Body Habits to Serum Insulin Concentrations: The Normative Aging Study., American Journal of Clinical Nutrition, 1993;58:129-136.

Pedersen, O., Beck-Nielsen, H., & Heding, L. Increased insulin receptors after exercise in patients with insulin-dependent diabetes mellitus. N Engl J Med 302:886-92, 1980.

Petry CJ et al., Early and late nutritional windows for diabetes susceptibility. Proc Nutr Soc, 56:233-42, 1997 Mar.

Pi-Sunyer FX. Weight and non-insulin-dependent diabetes mellitus. Am J Clin Nutr 1996;63(suppl):426S-9S.

Pizzorno, Joseph E. & Murray, Michael T. A Textbook of Natural Medicine. JBC Publications, Seattle, WA, 1985.

Pociot, F. et al: Nicotinamide - Biological Actions and Therapeutic Potential in Diabetes., Diabetologia, 1993;36:574-576.

References Q - Z

Raheja-BS: Diabetes and atherosclerosis as immune-inflammatory disorders: options for reversal of disease processes.. J-Assoc-Physicians-India. 1994 May; 42(5): 385-90, 395-6.

Rasmussen OW, Lauszus FF, Hermansen K. Effects of postprandial exercise on glycemic response in IDDM subjects. Diabetes Care 1994;17:1203.

Riales, R. & Albrink, M. Effect of chromium chloride supplementation on the glucose tolerance and serum lipids, including HDL, of adult men. Am J Clin Nutr 34:2670-8, 1981.

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

Robbins, S.L. & R.S. Cotran. 1979. Pathologic Basis of Disease. 2nd ed. Saunders Pub Co., Philadelphia. 1598 pp.

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.

Salmerion J et al., Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA, 277:472-7, 1997 Feb 12.

Sancetta, S.M., Ayres, P.R., & Scott, R.W. The use of vitamin B12 in the management of the neurological manifestations of diabetes mellitus, with notes on the administration of massive doses. Ann Int Med 35, 1951.

Schafer RG et al., Translation of the diabetes nutrition recommendations for health care institutions: technical review [see comments]. J Am Diet Assoc, 97:43-51, 1997 Jan.

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

Schroeder, H. The role of chromium in mammalian nutrition. Am J Clin Nutr 21:230-44, 1968.

Shaw, J.H. & E.A. Sweeney. 1978. Nutrition in relation to dental medicine. Modern Nutrition and Disease. 6th ed. Goodhart, R. S. and M. E. Shils, ed. Lea and Febiger.

Shoff, S. M. et al: Glycosylated Hemoglobin Concentrations and Vitamin E, Vitamin C and Beta-Carotene Intake in Diabetic and Nondiabetic Older Adults., American Journal of Clinical Nutrition, 1993;58:412-6.

Simpson, H.C.R., Simpson, R.W., Lousley, S., et al: A high carbohydrate leguminous fiber diet improves all aspects of diabetic control. Lancet 1:1-5, 1981.

Smith, U.: Insulin resistance in obesity, type II diabetes and stress. Acta Endocrin supp 262:67-9, 1984.

Sparks, S. P. et al: Blood Glucose Rise Following Prenatal Vitamins in Gestational Diabetes. Journal of the American College of Nutrition, 1993;12(5):543-546.

Spollett G: Diet strategies in the treatment of non-insulin-dependent diabetes mellitus. Lippincotts Prim Care Pract, 1:295-304; quiz 305-6, 1997 Jul-Aug.

Steinberg, M. Chromium deficiency and the glucose tolerance factor. J John Bastyr Coll Nat Med 1:32-6, 1979.

Stevens, E.J. et al: Prostacyclin Release in Experimental Diabetes: Effects of Evening Primrose Oil. Prostaglandins, Leukotrienes and Essential Fatty Acids, 1993;49:699-706.

Surwit, R. S.& Schneider, M. S.: Role of Stress in the Etiology and Treatment of Diabetes Mellitus. Psychosomatic Medicine, 1993;55:380-393.

Swanston-Flatt, S.K., Day, C., Flatt, P.R., Gould, B.J., Bailey, C.J.: Glycemic effects of traditional European plant treatments for diabetes. Studies in normal and streptozotocin diabetic mice. Diabetes Res. 10: 69-73, 1989.

Swanston-Flart, S.K et al., Traditional plant treatments for diabetes. Studies in normal and streptozotocin diabetic mice. Diabetologia 33: 462- 464, 1990.

Tadros, W.M., Awadallah, R., Doss, H., & Khalifa, K. Protective effect of trace elements (Zn, Mn, Cr, Co) on alloxan-induced diabetes. Ind J Exp Biol 20:93-4, 1982.

Takahashi, R., et al: Evening Primrose Oil and Fish Oil in Non-Insulin-Dependent Diabetes. Prostaglandins, Leukotrienes and Essential Fatty Acids, 1993;49:569-571.

Tarui, S. Studies of zinc metabolism: III. Effect of the diabetic state on zinc metabolism: A clinical aspect. Endocrinol Japan 10:9-15, 1963.

Tinker-LF et al: 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.

Toeller M et al., Nutritional intake of 2,868 IDDM patients from 30 centres in Europe. EURODIAB IDDM Complications Study Group. Diabetologia, 39:929-39, 1996 Aug.

Toeller M et al., Repeatability of three-day dietary records in the EURODIAB IDDM Complications Study. Eur J Clin Nutr, 51:74-80, 1997 Feb.

Uusitupa, M., Kumpulainein, J., Voutilainen, E., et al: Effect of inorganic chromium supplementation on glucose tolerance, insulin response, and serum lipids in noninsulin dependent diabetic. Am J Clin Nutr 38:404-10, 1983.

Vahouny, G. & Kritchevsky, D. Dietary Fiber in Health and Disease. Plenum Press, New York, NY, 1982.

Vallerand, A.L., Cuerrier, J.P., Shapcott, D., et al: Influence of exercise training on tissue chromium concentrations in the rat. Am J Clin Nutr 39:402-9, 1984.

Velussi, M. et al: Silymarin Reduces Hyperinsulinemia, Malondialdehyde Levels and Daily Insulin Need in Cirrhotic Diabetic Patients. Current Therapeutic Research, May 1993;53(5):533-545.

Vuorinen-Markkola, H. et al: Guar Gum and Insulin-Dependent Diabetes: Effects on Glycemic Control and Serum Lipoproteins., The American Journal of Clinical Nutrition, 1992;56:1056-60.

Wahlqvist ML: Nutrition and diabetes. Aust Fam Physician, 26:384-9, 1997 Apr.

Warshaw H et al., Fat replacers: their use in foods and role in diabetes medical nutrition therapy [see comments]. Diabetes Care, 19:1294-301, 1996 Nov.

Weitzman S: Nutrition and diabetes risk. Public Health Rev, 24:123-9, 1996.

Welihinda, J., Arvidson, G., Gylfe, E., et al: The insulin-releasing activity of the tropical plant Momordica charantia. Acta Biol Med Germ 41:1229-40, 1982.

Wheeler ML: A brave new world for nutrition and diabetes. Diabetes Care, 20:109-10, 1997 Jan.

Wiesemann A: Nutritional counseling in German general practices: a holistic approach. Am J Clin Nutr, 65:1957S-1962S, 1997 Jun.

Will JC & Byers T: Does diabetes mellitus increase the requirement for vitamin C? Nutr Rev, 1996 Jul, 54:7, 193-202.

Wimhurst, J.M. & Manchester, K.L. Comparison of ability of Mg and Mn to activate the key enzymes of glycolysis. FEBS Letters 27:321-6, 1972.

Wing RR, Marcuse MD, Blair EH, et al. Caloric restriction per se is a significant factor in improvements in glycemic control and insulin sensitivity during weight loss in obese NIDDM patients. Diabetes Care 1994;17:30.

Wing, R.R.: Use of very-low-calorie diets in the treatment of obese persons with non-insulin-dependent diabetes mellitus. J. Am. Diet. Assoc. 1995; 95:569-72.

Yudkin, J. Dietary factors in arteriosclerosis: Sucrose. Lipids 13:370-2, 1978.