Diabetes mellitus

Diabetes mellitus is a disease characterized by hyperglycemia resulting from a relative or absolute impairment in insulin secretion and the activity of insulin. Patients with type I diabetes mellitus (DM),also known as nsulin-dependent DM (IDDM) or juvenile-onset diabetes, are at risk of developing diabetic ketoacidosis (DKA). Patients with type II DM, also known as non-insulin-dependent DM (NIDDM), are at risk of developing hyperosmolar hyperglycemic nonketotic coma (HHNC). Common complications in both conditions include retinopathy, nephropathy,peripheral and autonomic neuropathies, as well as more overt indications of cardiovascular disease such as atherosclerosis. This condition relates to the effect of oxidizing effects of uncontrolled blood sugar and insulin upon cardiovascular tissue. Thus in IDDM, cardiovascular disease is the result of iatrogenesis, by recommending a high carbohydrate diet and the need for progressively larger amounts of injected insulin. (Berkow 1992, 1106-12; Rubin 2001,630-36)

Classification and pathogenesis

IDDM most commonly develops in childhood or adolescence and is the predominant type of DM diagnosed before age 30. This type of diabetes accounts for 10 to 15% of all cases of DM and is characterized clinically by hyperglycemia and a tendency to develop DKA. The pancreas produces little or no insulin. IDDM results from an immune-mediated, destruction of more than 90% of the insulin-secreting cells. The pancreatic islets of IDDM patients are inflamed, characterized by an infiltration of T lymphocytes accompanied by macrophages and B lymphocytes. The antibodies present at diagnosis usually become undetectable after a few years. (Berkow 1992, 1106-07)

Some researchers believe that susceptibility to IDDM is inherited as an autosomal dominant recessive trait, although fewer than 20% of these patients have a parent or sibling with the disease. Identical twin studies have cast further doubt on the idea that IDDM is an inherited disorder. Up to 95% of patients with IDDM express either HLA-DR3,HLA-DR4, or both, compared with only 20% of the population at large, which may suggest a susceptibility to IDDM. Given the inconclusive findings of genetic research however, environmental factors are still considered to be of prime importance, including viruses (congenital rubella, mumps, and coxsackie B viruses may incite the development of autoimmune -cell destruction) and exposure to cow’s milk (a specific sequence of albumin from cow’s milk may cross-react with islet protein). This latter factor may explain the very high incidence of IDDM in Scandanavian countries, for whom milk is not a traditional food. (Rubin 2001, 630)

NIDDM is usually diagnosed in patients older than 30 years of age, but is being diagnosed with increasing frequency in children and adolescents. It is characterized clinically by hyperglycemia and insulin resistance, and can be thought of as a worsening or progression of the same factors that promote metabolic yndrome. Such patients that are able to implement a strategy to lose truncal-abdominal weight and train muscle can be observed to have normal serum glucose levels. Some cases of NIDDM occur in young, nonobese adolescents (maturity-onset diabetes of the young [MODY]) with an autosomal dominant inheritance. Many families with MODY have a mutation in the glucokinase gene. (Rubin 2001, 632-33; Berkow 1992, 1109-10)

Chronic pancreatitis, particularly in alcoholics, is frequently associated with diabetes. Such patients lose both insulin-secreting and glucagon-secreting islets. These patients may be mildly hyperglycemic and sensitive to low doses of insulin. Given the lack of effective counterregulation (exogenous insulin that is unopposed by glucagon),they frequently suffer from rapid onset of hypoglycemia. In Asia, Africa, and the Caribbean, DM is commonly observed in young, severely malnourished patients with severe protein deficiency and pancreatic disease. NIDDM can be secondary to Cushing’s syndrome, acromegaly,pheochromocytoma, glucagonoma, primary aldosteronism, or somatostatinoma. Most of these disorders are associated with peripheral or hepatic insulin resistance. Many patients will become diabetic once insulin secretion is also decreased. The prevalence of NIDDM is increased in patients with certain autoimmune endocrine diseases, such as Graves’ disease, Hashimoto’s thyroiditis, and Addison’s disease (Rubin 2001, 632-33; Berkow 1992, 1109-10)

Diabetic ketoacidosis

IDDM is often first diagnosed with an emergency presentation from the effects of uncontrolled hyperglycemia and diabetic ketoacidosis (DKA). DKA is an acute, life threatening complication of uncontrolled IDDM in which there is a loss of urinary loss of water, potassium, ammonium and sodium, resulting in hypovolemia (decreased blood volume), electrolyte imbalance, very high blood glucose levels,and the breakdown of free fatty acids causing acidosis. (Rubin 2001, 632-33; Berkow 1992, 1122)

Ketoacidosis is an extension of normal physiological mechanisms that compensate for starvation. In the fasting state the body changes from metabolism based on carbohydrate, to the oxidation of fat. Free fatty acids produced in adipose cells are transported to the liver, bound to albumin, where they are broken down into acetate, and then turned into ketoacids (i.e. acetoacetate and beta-hydroxybutyrate). The ketoacids are then exported from the liver to peripheral tissues (notably brain and muscle) where they can be oxidized. During ketosis a relatively small amount of acetone is produced giving ketotic patients their typical odour, often described as ‘fruity’. DKA represents a derangement of this mechanism. Although there are large amounts of circulating glucose from the diet, it cannot be used owing to lack of insulin. Ketogenic pathways are thus initialized, but the supply of ketones soon exceeds peripheral utilization, and ketosis results. The resultant change in blood chemistry, called acidosis, is marked by an increase in hydrogen ion concentration and the widespread disruption of homeostatic mechanisms. Untreated, DKA leads to coma and death. DKA rarely occurs in NIDDM. (Berkow 1992, 1122)

Hyperosmolar hyperglycemic nonketotic coma

Patients with severe NIDDM are at risk for developing hyperosmolar hyperglycemic nonketotic coma (HHNC), a condition characterized by decreased consciousness, extreme dehydration and extremely high blood glucose levels. Normally the kidneys compensate for high glucose levels in the blood by excreting excess glucose in the urine. However, when water is scarce, the kidneys conserve fluid and glucose levels become higher, resulting in intracellular dehydration. Despite the name, coma is present in fewer than 10% of cases. HHNC most commonly develops in diabetic patients who have some concomitant illness that leads to a reduced fluid intake. (Berkow 1992, 1124-25)

Complications of diabetes mellitus

Complications only occur after several years of poorly controlled hyperglycemia, which, concomitant with insulin-resistance and compensatoryhyperinsulinema, results in both macro and microvascular damage see arterial disease). Macrovascular diseases such as atherosclerosis may lead to symptomatic coronary artery disease, claudication, skin breakdown, and infections. Amputation of a lower limb for severe peripheral vascular disease, intermittent claudication, and gangrene remains common. Background retinopathy can progress to macular edema or proliferative retinopathy with retinal detachment or hemorrhage, which can cause blindness. About 85% of all diabetics eventually develop some degree of retinopathy (e.g. age-related macular degeneration, AMD). (Rubin 2001, 633-36; Berkow 1992, 1109-11)

Diabetic nephropathy develops in about one third of IDDM patients and in a smaller percentage of NIDDM patients. Diabetic nephropathy is usually asymptomatic until end-stage renal disease develops, but it can cause nephrotic syndrome. (Rubin 2001, 633-36; Berkow 1992, 1109-11)

Diabetic neuropathy is characterized by a loss or reduction of sensation in the feet, and in some cases the hands, and pain and weakness in the feet. Nerve damage is likely due to a combination of factors, including hyperglycemia and hyperinsulinism, and ischemia. The symptoms of diabetic neuropathy are insidious and mild at onset,usually experienced as numbness, pain, or tingling in the hands, feet, or legs. After several years this may lead to weakness in the muscles of the feet. Occasionally, diabetic neuropathy can flare up suddenly and affect a specific nerve that may result in double vision or drooping of the eyelid, or weakness and atrophy of the thigh muscles. Nerve damage caused by diabetes generally occurs over a period of years and may lead to problems with internal organs including the digestive tract and sexual organs. These problems can then tend to cause indigestion, diarrhea or constipation, dizziness, bladder infections, and impotence. The loss of sensation in the feet is important as it may increase the possibility of injuries of which the patient is not aware. These foot injuries can develop into ulcers or lesions that can become infected. In some cases, ulcers may not heal and amputation may be required. (Rubin 2001, 633-36; Berkow 1992, 1109-11)

The risk of infection from fungi and bacteria is increased because of decreased cellular immunity caused by acute hyperglycemia and circulatory problems caused by chronic hyperglycemia. Peripheral skin infections and oral and vaginal thrush are most common. A fungal infection may be the initial pathogen, leading to lesions, cracks,fissures, and ulcerations that favor secondary bacterial invasion. Patients with infected foot ulcers frequently feel no pain because of neuropathy and have no systemic symptoms until late in the disease. (Rubin 2001, 633-36; Berkow 1992, 1109-11)

Diagnosis of diabetes

There are two primary methods of diagnosing diabetes: the fasting blood glucose (FBG) and the oral glucose tolerance test (OGTT). The FBG is a measurement of the blood glucose in a patient that has been fasting overnight (not eating anything after midnight). A value above 140 mg/dL on at least two occasions typically indicates diabetes: normal fasting blood sugar levels generally run between 70-110 mg/dL. Although this test is considered to the gold standard, it does not accurately indicate other problems with glucose metabolism, which can yield related diagnoses including hypoglycemia and insulin resistance that predispose a patient to diabetes. The other test that yields a broader perspective on the issue of glucose metabolism is the OGTT, usually given over three hours, but a six hour test is also used. In this test that patient begins the test in fasting state (having no food or drink except water for at least 10 hours but not greater than 16 hours), and an initial blood sugar reading is obtained. The patient is then given a premeasured volume of glucose in an oral form (75 g glucose, or 100 g in pregnant women). In the three hour test the patient then has their blood tested again in 30 minutes, 1 hour, 2 hours and 3 hours after drinking the high glucose drink. This test allows the physician to graph the blood glucose, to determine the effectiveness of glucose metabolism. (Rubin 2001, 633-36; Berkow 1992, 1109-11) Glucose tolerance tests may lead to one of the following diagnoses:

Normal response

  • A person is said to have a normal response when the 2-hour glucose level is less than 110 mg/dl.

Impaired fasting glucose

  • When a person has a fasting glucose greater than 110 mg/dl but less than 126 mg/dl they are said to have impaired fasting glucose. This is considered a risk factor for future diabetes, and the need for future testing.

Impaired glucose tolerance

  • A person is said to have impaired glucose tolerance when the 2-hour glucose results from the oral glucose tolerance test are greater than or equal to 140 but less than 180 mg/dl.


  • A person has diabetes when oral glucose tolerance tests show that the blood glucose level at 2 hours is equal to or more than 180 mg/dl. This is usually confirmed by a second test on another day. (Rubin 2001, 633-36; Berkow 1992, 1109-11)

Medical treatment

The medical management of diabetes consists of dietary changes, the use of hypoglycemic drugs, and in progressed conditions, insulin by injection. Dietary changes are the typical high-complex carbohydrate/low fat and salt recommendations that have remained unchanged over the last 20 years despite the fact that the prevalence of cardiovascular disease, obesity and diabetes has increased significantly. Some medical texts such as the Merck Manual still emphasize the benefit of hydrogenated fatty acids over saturated fat despite all the evidence to the contrary.

The most commonly used hypoglycemic drug in NIDDM is metformin (glucophage®), typically prescribed at the time of diagnosis. Metformin is a biguanide, a synthetic compound originally derived from guanides in Goat’s Rue (Galega officinalis). Metformin exerts its benefits by enhancing peripheral glucose utilization in muscle. Side effects include diarrhea, abdominal discomfort and nausea, and because the drug is excreted by the kidneys it can accumulate in renal failure and promote lactic acidosis. Metformin has in large part replaced the older drugs is types of drugs such as the sulfonylureas (e.g. glyburide [diamicron®]), which act as insulin secretogogues.

Another, newer class of drugs are the thiazolidinediones, such as troglitazone (rezulin®), that sensitize muscle, fat and to lesser extent liver cells to the actions of insulin. If the sulfonylureas and metformin fail to adequately manage the blood glucose the patient is then prescribed a thiazolidinedione on top of the other drugs, or is given a drug such as glargine or insulin (by injection) at bedtime to control fasting glucose levels. Unless proper dietary changes are implemented and nutritional deficiencies accounted for however, virtually all patients with NIDDM become insulin deficient, and thus will eventually require insulin. (Berkow 1992, 1112-20; Quinn 1997; Bernstein 1997, 191-252)

Insulin preparations varies depending upon numerous factors, including the type, strength and duration of action. Since William Banting developed the first insulin treatment in the early 1900’s, drug companies have fought an intense battle over this very lucrative market, and have developed a number of different types of insulins,derived from animal sources (e.g. porcine, bovine) or by using recombinant DNA technology (from bacteria or yeasts). The primary difference between them is what other ingredients are contained in the preparation, which affects the potency and duration of action. To delay the activity of insulin it is combined with either a protein called protamine (derived from fish sperm) or zinc crystals – some have criticized the use of protamine as a suspension agent however,as it has a greater potential to be recognized as antigenic by immune cells, which can bind to the insulin, deactivate it and play havoc with maintaining proper blood sugar levels. (Berkow 1992, 1114; Bernstein 1997, 210-11)

The amount of the suspending agent in insulin affects the onset, peak activity and duration of activity. Generally, insulin preparations are either rapid-acting (15-30 minutes), intermediate-acting (1-2 hours), or long-acting (4-8 hours). Rapid-acting insulins achieve peak activity within 2-4 hours and last between 6-8 hours,and are injected about 40 minutes before meals to prevent blood sugars from rising after meals. Intermediate-acting insulins (e.g. NPH, Lente®) achieve peak activity within 6-12 hours and last between 18-26 hours, are given at the beginning of the day, usually 30-60 minutes before breakfast. Long-acting insulins (e.g. Ultralente®, PZI) achieve peak activity within 12-24 hours and last between 28-36 hours, and are given at night just before bed, to keep blood sugar levels from rising while sleeping. In practice, many insulin-dependent diabetics will inject a combination of rapid-acting and intermediate insulin (e.g. 70/30, 50/50), although some experts such as Dr. Richard Bernstein suggest that these ‘all-in-one’ approaches rarely achieve the kind of meticulous control over blood sugar that is required to avoid the complications of diabetes.(Berkow 1992, 1114-15; Bernstein 1997, 210-15) Except in emergency situations, an insulin regimen is only instituted or changed according to the blood sugar data, which ideally, should be a record of the blood sugar over an entire day for a minimum of one week. This data is collected with the use of a glucometer, a monitor with a spring loaded device with which a lancet is loaded, the skin pricked, and a drop of blood squeezed onto a chemical reagent strip or a strip that has tiny electrodes, both of which respond to changes in blood sugar. This strip is then fed into the monitor, which reads these changes and outputs the reading to an LCD monitor. Typically, the hands are used for obtaining a sample of blood, best obtained from the dorsal surfaces of the fingers, behind the fingernail or the first finger joint (if palmar surfaces are used, they can eventually become callused). Lancets can be used several times, but should be disposed of at least every week because they become dulled over time. (Bernstein 1997, 67-73)

While some of the newer glucometers have a memory chip that allows them to record successive blood sugar readings, the data is best recorded on a chart, on which other notes can be made. If the patient is taking insulin twice a day (AM and PM), the blood sugar should be monitored up to five times a day:

  1. on an empty stomach, first thing in the morning
  2. two hours after breakfast
  3. two hours after lunch
  4. wo hours after supper
  5. before bed (Bernstein 1997, 73)

Besides the blood sugar data, patients should also record:

  1. when and what they are eating at each meal
  2. when and which medication they are taking (e.g. metformin, insulin)
  3. the timing and duration of any exercise
  4. any symptoms (Bernstein 1997, 73)

Most medical texts suggest that blood sugar levels should be maintained between 80 and 150 mg/dL, but in order to prevent the complications associated with diabetes the blood sugar should be no more than any normal person’s fasting sugar, which is less than 110 mg/dL. Hypoglycemia is a life-threatening problem in insulin-dependent diabetics, and is classified as less than 50 mg/dL in men, 45 mg/dL in women, and 40 mg/dL in children – in long-standing, poorly controlled diabetes however even modest decreases in blood sugar can promote uncomfortable symptoms. Symptoms of hypoglycemia include confusion, blurred/double vision, headache, tremors, tingling, numbness, tinnitus, hunger, elevated pulse rate, clumsiness,irritability, restlessness, anxiety, weakness, light-headedness, rapid/shallow breathing, nausea, slurred speech, coldness or feeling too hot, nystagmus, stupor, seizures and coma. Episodic hypoglycemia is treated by ingesting glucose tablets to raise the blood sugar to 60 mg/dL – in the average 140 lb adult, one gram of glucose will raise the blood sugar 5 mg/dL. In cases where insulin doses are too high, they are adjusted in 10% increments over a three day period, while carefully monitoring the blood sugar. While injecting too much insulin or taking too high a dose of insulin-promoting drugs such as diamicron can cause hypoglycemia, other causes include not eating enough, skipping meals and drinking too much alcohol (esp. before meals). Gastroparesis or delayed stomach emptying is another cause of hypoglycemia, which makes it difficult to predict blood sugar levels after eating – in diabetic patients gastroparesis is a manifestation of a more generalized diabetic neuropathy (which includes other signs such as dry feet, peripheral numbness, poor reflexes, foot pain etc.). (Berkow 1992, 1114-16, 1129; Berstein 1997, 253-61, 283)

Holistic treatment

The holistic treatment of NIDDM is essentially the same as for metabolic syndrome, with the addition of a few key nutrients and herbs, and specialized approaches to deal with the complications of diabetes. In this respect, NIDDM is simply a progression of metabolic syndrome, and in a similar fashion will often display the cardiovascular changes seen in metabolic syndrome but in a more progressed state. Holistic treatment seeks to replace the many drugs used in managing NIDDM by first implementing the necessary dietary changes, and thereafter gradually reducing drug dosage and replacing these with natural products that have similar hypoglycemic properties. As most NIDDM patients are already suffering from compromised cardiovascular function and on drug treatment for dyslipidemia and hypertension, treatment protocols for atherosclerosis should be carefully reviewed and implemented. In NIDDM patients the administration of insulin should be avoided at all costs through proactive measures as it simply exacerbates the underlying pathology and increase morbidity and mortality. The treatment of NIDDM is as follows:

1. Dietary changes.

  • implement a very low carbohydrate diet to reduce the need for insulin
  • eliminate grain-fed animal products, transfatty acids, and refined oils
  • strictly avoid all sweets, sweeteners, refined carbohydrates and most tropical fruits (half-sweet tropical fruits such as guava, starfruit and passionfruit may be acceptable, as well as temperate fruits such as blueberries, strawberries and raspberries)

2. Supplement for key nutrient deficiencies

  • omega-3 fatty acids, EPA/DHA, equal to 1000 mg each, daily
  • vitamin B complex, 100 mg daily
  • vitamin D3, 3000-5000 IU daily
  • magnesium, 800-1200 mg daily
  • manganese,20-50 mg daily
  • chromium,200 mcg, thrice daily, with meals
  • zinc,50 mg daily
  • vanadium, 75 mcg, thrice daily, with meals

3. Botanical support for the pancreas and liver

  • Devil’s Club (Oplopanax horridum), Ginseng (Panax spp. (all)), Gudmar (Gymnema sylvestre), Fenugreek (Trigonella foenum-graecum), Bitter Melon (Momordica charantia), Turmeric (Curcuma longa), Reishi (Ganoderma lucidum), Milk Thistle (Silybum marianum), Hu Huang Lian (Picrorrhiza scrophulariae), Triphala, Shilajitu
  • raw garlic and onions can significantly lower blood sugar

4. Treat gastroparesis to manage blood sugar levels

  • digestive enzymes
  • dipanapachana, to enhance agni: Pippali (Piper longum), Ginger (Zingiber officinalis), Black Pepper (Piper nigrum), Fennel (Foeniculum vulgare), Cardamom (Elettaria cardamomum), Ajwan (Trachyspermum ammi)
  • strengthen the Spleen Qi, to relieve Food Stagnation: Dang Shen (Codonopsis pilosula), Huang Qi (Astragalus membranaceus), Ginseng (Panax spp), Shan Za (Crataegus pinnatifida), Chen Pi(Citrus reticulata)
  • gastric tonics, to stimulate HCl production: Barberry (Berberis vulgaris), Yellow Gentian (Gentiana lutea), Centuary (Centaurium erythraea), Buckbean (Menyanthes), Goldenseal (Hydrastis canadensis)

5 .Support cardiovascular function

  • review holistic treatment under arterial disease
  • implement antioxidant therapy

6.Treat neuropathy, if present

  • nervine trophorestoratives: Ashvagandha (Withania somnifera), Shatavari (Asparagus racemosa), Ginseng (Panax spp), Milky Oats (Avena sativa), Shilajatu, Gotu Kola (Centella asiatica), Siberian Ginseng (Eleuthrococcus senticosis), Damiana (Turnera diffusa), Bala (Sida cordifolia), Amalaki (Phyllanthus emblica)
  • Antioxidant botanicals: Turmeric (Curcuma longa), Frankincense (Boswellia thurifera), Guggulu (Commiphora mukul), Reishi (Ganoderma lucidum), Caterpillar Fungus (Cordyceps), Maitake (Grifolia frondosa), Turkey Tail Mushroom (Trametes versicolor), Hawthorn (Crataegus oxyacantha),Amalaki (Phyllanthus emblica), Brahmi (Bacopa monniera), Guduchi (Tinospora cordifolia), Ginkgo(Ginkgo biloba), Rosemary (Rosmarinus officinalis), Gotu Kola (Centella asiatica), Milk Thistle (Silybum marianum), Chai Hu (Buplerum chinense), San Qi (Panax notoginseng) formulae:Yogaraja guggulu
  • alpha lipoic acid


  • implement a muscle-building regimen to decrease insulin resistance, i.e. anaerobic exercise (e.g. weight lifting, calisthenics, martial arts,hiking, bicycling etc.) as opposed to aerobic exercise (e.g. jogging, aerobics tc.); minimum one hour daily exercise can be just as effect as oral hypoglycemics to bring an immediate decrease in blood sugar