|
|
|
Overview |
|
|
Definition |
|
Diabetes mellitus results from the body's failure to regulate blood glucose
levels adequately. It is a common endocrine disease, with more than 600,000 new
cases diagnosed in the United States each year. It affects men and women of all
ages, races, and income levels. Among those over 40, it affects 1:15 Caucasians
and 1:10 to 1:8 African-Americans and Hispanics. Among those over 65, 1 of every
5 persons has diabetes and up to 50% of patients are undiagnosed. There is a
strong familial susceptibility to the condition. Two major forms are
seen:
- Type I (insulin-dependent diabetes mellitus [IDDM]): usually occurs
before age 30, most likely between ages 11 and 13; accounts for about 10% of
cases.
- Type II (non-insulin-dependent diabetes mellitus [NIDDM]): usually
occurs in those over age 40; accounts for about 90% of cases; 30% to 40% need
insulin.
Gestational diabetes (GDM) can occur in pregnant women. Diabetes can be
secondary to pancreatic disease, the use of chemicals or drugs, various genetic
syndromes (Turner's syndrome, myotonic dystrophy, or Prader-Willi syndrome),
rare abnormalities in the cellular receptor for insulin, or an autosomal
dominant inherited disorder. |

|
|
Etiology |
|
Unknown, but most likely a combination of genetic predisposition, viral
infection, lifestyle, nutrition and diet, obesity, autoimmune disorders, and
exposure to toxic agents. Type I probably results when pancreatic beta cells are
attacked and destroyed by an autoimmune process triggered by a viral infection
in a genetically susceptible individual. Type II develops in older, overweight
individuals whose insulin production is insufficient to meet body needs or whose
response to insulin is diminished by a loss of insulin receptors on the surface
membranes of target cells. |

|
|
Risk Factors |
|
Type I:
- Family history of diabetes, thyroid disease, or other
endocrinopathies
- Family history of autoimmune diseases such as Hashimoto's
thyroiditis, Graves' disease, myasthenia gravis, or pernicious anemia
- Cow's milk consumption in infancy
Type II:
- Obesity and age over 40 years
- Family history of diabetes, thyroid disease, or other
endocrinopathies
- Sedentary lifestyle with diet high in fats and calories
- African-American, Hispanic, American Indian, or Asian or Pacific
Island-American
|

|
|
Signs and Symptoms |
|
- Polyuria, polydipsia, rapid weight loss, and hyperglycemia
- Glycosuria
- Increased susceptibility to infection
- Dehydration
- Polyphagia
- Fatigue or weakness
- Blurred vision
- Stiffness in the shoulder and upper back
- Pruritus, numbness, and tingling in the hands and feet
- Leg cramps
- Hyperlipidemia
- Ketoacidosis
|

|
|
Differential
Diagnosis |
|
- Polydipsia—medication side effect,
psychogenic factors, diabetes insipidus
- Polyuria—hypercalcemia, medication side
effect, renal wasting, urologic or prostate conditions
- Blurred vision—myopia, presbyopia
- Fatigue or weakness—thyroid disorder,
anemia, adrenal insufficiency, depression
- Pruritus—allergy, renal failure
- Cushing's disease
- Corticosteroid use
|

|
|
Diagnosis |
|
|
Physical Examination |
|
Patient may present with fatigue, lethargy, poor concentration, and atypical
thirst for liquids. |

|
|
Laboratory Tests |
|
- Two or more fasting plasma glucose levels over 140 mg/dL or one level
over 200 mg/dL plus other signs and symptoms.
- Oral glucose tolerance test values 120 to 140 mg/dL
- Glycosylated hemoglobin test showing consistently elevated
values.
- Glycosylated hemoglobin is used to track treatment efficacy, not to
diagnose DM.
|

|
|
Pathology/Pathophysiology |
|
Elevated blood sugar levels with weight loss, decreased blood pressure,
nonhealing wounds (especially on the extremities), recurrent cutaneous
infections, decreased extremity sensation, retinal abnormalities or cataract
formation, carotid bruits, abdominal tenderness, dry skin, and hair loss over
lower leg and foot. |

|
|
Other Diagnostic
Procedures |
|
Blood glucose testing |

|
|
Treatment Options |
|
|
Treatment Strategy |
|
- Control blood sugar levels; helps reduce complications.
- Requires patients to be self-disciplined, able to concentrate, able
to maintain a positive attitude, and honest with self and physician.
- Components are diet, exercise, blood glucose self-monitoring, oral
hypoglycemic agents (Type II), and insulin (Type I).
- Because diabetes affects so many body systems, treatment planning
must include a whole-body approach.
Treatment specific to Type I:
- Diet—consistent timing/content (same gram
amount of carbohydrates, protein, and fat at each meal); consult dietitian for
meal planning.
- Exercise—daily; wear proper shoes and
protective equipment; avoid extreme heat or cold; check feet daily and after
exercise; suspend exercise when blood glucose control is poor.
- Self-monitoring—teach the patient to use a
home glucose meter and make needed adjustments in diet, exercise, and/or
insulin.
Treatment specific to Type II:
- Diet—use moderation; lose weight by
decreasing calories while increasing activity; base choices on USDA Food
Pyramid.
- Exercise—as for Type I; do moderate aerobic
exercise (50% to 70% of VO2 max) for 20 to 45 minutes at least three
days a week; include low-intensity warm-up and cool-down exercises.
- Self-monitoring—as for Type I, with
adjustments in diet, exercise, and/or oral hypoglycemic agent as
needed.
|

|
|
Drug Therapies |
|
Insulin (used for Type I and occasionally Type II [30% to 40%]). Taken
subcutaneously, with dose and type individualized to the patient's condition.
Possible treatment regimens:
- Three-injections/day, doses adjusted to variations in
control
- Long-acting and short-acting preparations taken at meals for stable
background levels
- External insulin pump for tight control
- Single injection/day for those with some pancreatic
function
Sulfonylureas (Type II only). Oral hypoglycemic agents used when diet and
exercise are ineffective or in conjunction with diet and exercise. Doses
individualized to the patient's condition. Side effects include hypoglycemia,
nausea, heartburn, stomach fullness; intolerance and allergy (<2% of
patients). Use with caution in persons with liver or kidney impairment and those
with sulfa allergy. Approved agents:
- Acetohexamide (Dymelor)—250 to 1,500 mg;
slight diuretic effect
- Chlorpropamide (Diabinese, Glucamide)—100 to
750 mg; very long duration of action, antidiuretic effect
- Tolazamide (Tolinase)—100 to 1,000 mg;
slight diuretic effect
- Tolbutamide (Orinase)—500 to 3,000 mg;
usually taken in two to three doses/day
- Glipizide (Glucotrol)—5 to 40 mg; take on
empty stomach
- Glipizide-extended release (Glucotrol XL)—20
mg; do not break tablet, take once/day
- Glyburide (Diabeta, Micronase)—1.25 to 30
mg
- Glyburide-micronized (Glynase)—12 mg/day;
not equivalent in action to glyburide
- Glimepiride (Amaryl)—8 mg/day
- Metformin (Glucophage)—Used as a supplement
to or substitute for sulfonylureas. Side effects include weight loss, nausea,
abdominal discomfort, and diarrhea. Use with caution in persons with conditions
leading to lactic acid buildup (congestive heart failure, severe vascular
disease, kidney or liver disease). Discontinue 24 to 48 hours before surgery or
radiographic dye study. Dose: 1 to 2.5 g/day in two to three doses; available in
500 and 850 mg tablets; take before meals
- Acarbose (Precose)—Slows absorption of
carbohydrate into blood, acts locally in the intestine. Take at the beginning of
a meal for immediate action. Major side effect is increased gas production (up
to 75% of users). Dose: 50 to 100 mg depending on results and side
effects
- Troglitazone (Rezulin)—In trials for use
with insulin; liver damage reported
- Repaglinide (Prandin)—Meglitinide class; use
in Type II disease
|

|
|
Complementary and Alternative
Therapies |
|
Treatments stabilize blood sugars. Also, alternative therapies have an
important role in preventing vascular damage and some of the serious
complications that may be involved with DM. A combination of herbs and
nutrition, along with lifestyle changes, can be quite helpful. Regular exercise
is extrememly important. Ten minutes/day of exercise has been shown to have an
effect on glucose tolerance, although a minimum of 30 minutes three times/week
is required to see significant changes. Extended exercise is desired. Short
bursts of activity may actually increase glucose levels. |

|
|
Nutrition |
|
- Diet: the classic diet for DM is high in complex carbohydrates and
fiber. Some people, however, achieve better glucose control with a high-protein
diet with very few carbohydrates. If the classic diet does not stabilize blood
sugar, a trial of high-protein diet may be indicated.
- Essential fatty acids: anti-inflammatory, decrease insulin
resistance, and prevent cardiovascular and neurological complications of DM.
Evening primrose oil (2,000 mg bid) or fish oil (1,200 mg bid) rather than flax
or borage may be required, since a greater percentage of diabetics are lacking
enzymes required for utilization of flax and/or borage oil.
- OPCs (oligomeric procyanidins) such as pycnogenol or grape seed
extracts help to support vascular health and prevent oxidation side effects
associated with diabetes
- B-complex: biotin (300 mcg), B1 (50 to 100 mg), B2 (50 mg), B3 (100
mg), B6 (50 to 100 mg), B12 (100 to 1,000 mcg), folate (400 mcg/day) help
prevent neuropathy, control glucose levels, and prevent nephropathy
- Vitamin C (2 to 3 g/day) may prevent microangiopathy and
hypertriglyceridemia
- Vitamin E (400 IU/day) may reduce insulin requirements so should
start at 100 IU and gradually increase the dose; enhances healing of ulcers, and
is a cardioprotective antioxidant
- Brewer's yeast: contains chromium, which may improve glucose
tolerance, and glutathione, an antioxidant (9 g or 3 tbsp. brewer's yeast/day
and/or 200 mcg chromium)
- Magnesium: (400 mg/day) low in diabetics, may help prevent the
calcium deposition in arterial walls
- Manganese: (500 to 1,000 mcg) low in diabetics, may help stabilize
glucose levels
- Zinc: (30 mg/day) may decrease fasting glucose levels and help
prevent fatty acid oxidation
- Coenzyme Q10: (50 to 100 mg bid) depleted by oral hypoglycemic
agents, prevents fatty acid oxidation
- Vanadium: (5 to 10 mg/day) to normalize serum cholesterol and
triglycerides
- Some feel that chromium picolinate (200 mcg) helps normalize sugar
metabolism.
|

|
|
Herbs |
|
Herbs are generally a safe way to strengthen and tone the body's systems.
Ascertain a diagnosis before pursuing treatment. Herbs may be used as dried
extracts (capsules, powders, teas), glycerites (glycerine extracts), or
tinctures (alcohol extracts). Unless otherwise indicated, teas should be made
with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or
flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be
used singly or in combination as noted.
- Garlic (Allium sativum) increases fibrolysis, inhibits
platelet aggregation, lowers lipids
- Onion (Allium cepa) lowers lipids and blood pressure, inhibits
thrombocyte aggregation
- Bilberry (Vaccinium myrtillus) is a flavonoid, historic use in
DM, especially to prevent diabetic retinopathy
- Fenugreek (Trigonella foenum-graecum) historically used to
stabilize blood sugar
- Garlic and onions should be consumed liberally in the diet; bilberry
and fenugreek, equal parts, can be used as 1 cup tea tid or 30 to 60 drops
tincture tid
- Cayenne (Capsicum annum): 0.075% capsaicin cream topically,
decreases pain in peripheral neuropathy after two to four weeks of
use
|

|
|
Homeopathy |
|
An experienced homeopath should assess individual constitutional types and
severity of disease to select the correct remedy and potency. Constitutional
homeopathy may be helpful. |

|
|
Acupuncture |
|
May be helpful in both symptomatic relief and increasing overall
vitality. |

|
|
Massage |
|
May be helpful in relieving stress, which decreases cortisol and stabilizes
blood sugar, and for maintaining healthy circulation in the
extremities. |

|
|
Patient Monitoring |
|
- Patients taking insulin—daily fingerstick to
measure blood sugar levels, weight, and skin evaluation (redness indicating
allergy to insulin, edema, or cellulitis)
- Electrocardiogram at initial visit
- Thyroid-stimulating hormone and thyroid antibody screening for
high-risk patients at initial visit and then as indicated by antibody tests and
physical examination
- Lipid profile four to six weeks after beginning therapy and three
months later
- Every three months: glycosylated hemoglobin or hemoglobin A, urine
dipstick, LFT
- Yearly: 24-hour urine collection to measure microalbumin, protein,
creatinine clearance rate; electrolytes, BUN, dilated funduscopic
examination
- Yearly: opthalmology exam, foot
exam
|

|
|
Other
Considerations |
|
|
Prevention |
|
Avoid weight gain and obesity. Maintain regular physical
activity. |

|
|
Complications/Sequelae |
|
- Diabetic ketoacidosis
- Hyperosmolar coma
- Arteriosclerosis—cardiac, peripheral
vascular, or cerebrovascular disease
- Diabetic eye disease—glaucoma, cataracts,
blindness
- Diabetic kidney disease—nephropathy,
failure
- Diabetic neuropathy—peripheral symmetrical
polyneuropathy, autonomic neuropathies, mononeuropathies
- Foot ulcers/infections
- Skin changes—bruising, hypertrophy, or
lipoatrophy at injection site, dryness, fungal infections, vitiligo, necrobiosis
lipoidica diabeticorum, pruritus, alopecia, scleroderma adultorum, xanthomas,
xanthelasma, acanthosis nigricans, gangrene, skin ulcers
- Musculoskeletal problems—stiff joints, tendon
contractures of the hands, bursitis
|

|
|
Prognosis |
|
Prevent and/or slow development of complications by maintaining blood glucose
averages around 155 mg/dL. Complications usually begin 10 to 20 years after
onset of disease. |

|
|
Pregnancy |
|
Women of child-bearing age with diabetes should consult an endocrinologist
about the benefits of tight glucose control before attempting conception. Target
blood glucose concentrations are:
- Fasting: 60 to 90 mg/dL (3.3 to 5 mmol/L)
- Preprandial: 60 to 105 mg/dL (3.3 to 5.8 mmol/L)
- Two hours postprandial: 90 to 120 mg/dL (5 to 6.7
mmol/L)
Women with gestational diabetes should be treated to normalize glucose levels
and reduce the risk of complications (developmental malformations, perinatal
morbidity/mortality). Modify diet to improve glucose values. If this fails, use
insulin therapy; oral hypoglycemic agents are contraindicated during pregnancy.
Subsequent pregnancies can be affected, and risk of developing type II diabetes
is increased. If maternal glucose levels uncontrolled, infant can suffer CNS
defects, macrosomia, organomegaly, cardiac or renal anomalies, situs inversus,
stillbirth, asphyxia, respiratory distress, increased blood volume,
hyperviscosity, congestive heart failure, hypocalcemia, hypomagnesemia,
hypoglycemia, or hyperbilirubinemia. |

|
|
References |
|
Anderson RA, Cheng N, Bryden NA, et al. Elevated intakes of supplemental
chromium improve glucose and insulin variables in individuals with type 2
diabetes. Diabetes. 1997;46:1786-1791.
Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic
Guide to Herbal Medicines. Boston, Mass: Integrative Medicine
Communications; 1998:134, 176.
Boden G, Chen X, Igbal N. Acute lowering of plasma fatty acids lowers basal
insulin secretion in diabetic and nondiabetic subjects. Diabetes.
1998;47:1609-1612.
Cohen N, Halberstam M, Shlimovich P, Chang CJ, Shamoon H, Rossetti L. Oral
vanadyl sulfate improves hepatic and peripheral insulin sensitivity in patients
with with non-insulin-dependent diabetes mellitus. J Clin Invest.
1995;95:2501-2509.
Gruenwald J, Brendler T, Jaenicke C, et al., eds. PDR for Herbal
Medicines. Montvale, NJ: Medical Economics Co; 1998:1201.
Hirsch IB, Atchley DH, Tsai E, et al. Ascorbic acid clearance in diabetic
nephropathy. J Diabet Complications. 1998;12:259-263.
Koutsikos D, Agroyannis B, Tzanatos-Exarchou H. Biotin for diabetic
peripheral neuropathy. Biomed Pharmacother. 1990;44:511-514.
Noble J. Textbook of Primary Care Medicine. 2nd ed. St Louis, Mo:
Mosby-Year Book; 1996.
Perossini M, et al. Diabetic and hypertensive retinopathy therapy with
Vaccinium myrtillus anthocyanosides (Tegens): double blind placebo controlled
clinical trial. Annali di Ottalmaologia e Clinica Ocaulistica.
1987;CXII.
Poucheret P, Verma S, Grynpas MD, McNeill JH. Vanadium and diabetes. Mol
Cell Biochem. 1998;188:73-80.
Tandan R, et al. Topical capsaicin in painful diabetic neuropathy. Controlled
study with long-term follow-up. Diabetes Care. 1992;15:8-14.
Thibodeau GA, Patton KT. Anatomy and Physiology. 4th ed. St Louis, Mo:
Mosby-Year Book; 1999.
Tierney LM Jr, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and
Treatment. 33rd ed. Norwalk, Conn: Appleton & Lange; 1994.
Ziegler D, Hanefeld M, Ruhnau KJ, et al. Treatment of symptomatic diabetic
peripheral neuropathy with the anti-oxidant alpha-lipoic acid. A 3-week
randomized controlled trial. Diabetologia. 1995;38:1425-1433.
Ziegler D, Schatz H, Conrad F, Gries FA, Ulrich H, Reichel G. Effects of
treatment with the antioxidant alpha-lipoic acid on cardiac autonomic neuropathy
in NIDDM patients. A 4-month randomized controlled multicenter trial.
Diabetes Care.
1997;20:369-373. |

|
Copyright © 2000 Integrative Medicine
Communications This publication contains
information relating to general principles
of medical care that should not in any event be construed as specific
instructions for individual patients. The publisher does not accept any
responsibility for the accuracy of the information or the consequences arising
from the application, use, or misuse of any of the information contained herein,
including any injury and/or damage to any person or property as a matter of
product liability, negligence, or otherwise. No warranty, expressed or implied,
is made in regard to the contents of this material. No claims or endorsements
are made for any drugs or compounds currently marketed or in investigative use.
The reader is advised to check product information (including package inserts)
for changes and new information regarding dosage, precautions, warnings,
interactions, and contraindications before administering any drug, herb, or
supplement discussed herein. | |