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Look Up > Conditions > Hypoglycemia
Risk Factors
Signs and Symptoms
Differential Diagnosis
Physical Examination
Laboratory Tests
Other Diagnostic Procedures
Treatment Options
Treatment Strategy
Drug Therapies
Complementary and Alternative Therapies
Patient Monitoring
Other Considerations


Hypoglycemia is characterized by an inadequate concentration of glucose in circulating blood (low blood sugar). Beta cells in the pancreas secrete the hormone insulin after meals in response to an increase in plasma glucose concentrations. Insulin, in turn, lowers plasma glucose concentrations by increasing the rate at which glucose is taken up by cells. A deficiency of plasma glucose (e.g., after exercise, during pregnancy) because of increased glucose utilization causes the alpha cells of the pancreas to secrete the hormone glucagon. Glucagon, in turn, stimulates the release of glucose that is stored in the liver as glycogen to make up for the deficit. These glucoregulatory mechanisms can become overworked by lifestyle factors such as stress or poor diet, or by disease, or as a result of genetic predisposition.

Hypoglycemia is typically divided into two categories: fasting (postabsorptive) hypoglycemia and reactive (postprandial) hypoglycemia. Fasting hypoglycemia is associated with medications (e.g., sulfonylureas) and serious disease states (e.g., critical organ failure, various cancers, prolonged starvation). Reactive hypoglycemia is associated with postprandial hypoglycemia that becomes symptomatic several hours after a meal, and often with exercise. It is usually not associated with a serious preexisting disorder.


Reactive causes include:

  • Fasting hypoglycemia
  • Prolonged starvation
  • Postprandial hypoglycemia, especially with exercise
  • Gastric surgery

Fasting (postabsortive) causes include:

  • Drugs (e.g., insulin, sulfonylureas, alcohol)
  • Organ failure (e.g., renal, cardiac, or hepatic failure)
  • Hormone deficiencies (e.g., growth hormone, cortisol)
  • Endogenous hyperinsulinism (e.g., insulinoma)
  • Non-beta cell tumors (e.g., fibrosarcoma, mesothelioma)
  • Congenital enzyme abnormalities (e.g., glycogen storage disease type 1)

Risk Factors
  • Diabetes (especially insulin excess and impaired glucose counter-regulation)
  • Excessive use of alcohol, tobacco, coffee, or caffeine-containing drinks
  • Treatment for diabetes (e.g., sulfonylureas)
  • Cancer
  • Poor diet (e.g., excessive intake of simple carbohydrates and/or inadequate protein intake)
  • Congenital enzyme abnormalities
  • Severe illness (e.g., organ failure, sepsis)

Signs and Symptoms

Clinical manifestations of low glucose levels are nonspecific but can range from mild (subtle impairment) to severe and life-threatening (coma, death). Because glucose is critical for proper brain function, low levels manifest in the brain first.

  • Headache
  • Depression, anxiety
  • Palpitations
  • Bizarre behavior, mental confusion
  • Blurred vision, vertigo
  • Excessive sweating
  • Tremulousness, incoordination
  • Slurred speech
  • Seizures (common in children but rare in adults)
  • Fatigue
  • Coma
  • Irritability

Differential Diagnosis
  • Diabetes
  • Depression
  • Premenstrual syndrome and menopause
  • Central nervous system tumors or abnormalities
  • Psychiatric disturbances
  • Dumping syndrome

Physical Examination

Hypoglycemia is most often suspected on the basis of the history or the presenting symptoms which may include irritability, confusion, tremulousness, diaphoresis, and tachycardia. Screening laboratory tests are essential. The diagnosis of hypoglycemia is based on Whipple's triad: symptoms of hypoglycemia, low plasma glucose concentrations, relief of symptoms when normal plasma glucose levels are restored.

Laboratory Tests
  • Blood and plasma glucose
  • Serum insulin, calcium, phosphate, uric acid, lipids, creatinine
  • Liver tests
  • Insulin antibodies
  • Plasma and urine corticosteroids

  • Fasting plasma glucose levels of 60 to 105 mg/dL are normal.
  • Fasting plasma glucose levels of 45 to 60 mg/dL suggest hypoglycemia.
  • Fasting plasma glucose levels less than 45 mg/dL indicate severe hypoglycemia
  • Fasting plasma glucose levels over 140 mg/dL indicate diabetes.


Computed tomography (CT) scans are used to diagnose non-beta cell tumors, insulinomas, or other tumors that may be responsible for hypoglycemia.

Other Diagnostic Procedures
  • Glucose tolerance test (GTT [fasting])
  • Glucose-insulin tolerance test (G-ITT)
  • Hypoglycemic index (e.g., calculation of the fall in blood glucose 90 minutes before the nadir divided by the value of the nadir; a hypoglycemic index >O.8 indicates reactive hypoglycemia)
  • Symptom assessment
  • C-peptide suppression test
  • Glucose infusion test
  • Measurement of counter-regulatory hormone concentrations

Treatment Options
Treatment Strategy

Fasting hypoglycemia can be a medical emergency because of the adverse effects of prolonged low blood sugar on the brain, whereas reactive hypoglycemia is usually self-limited and rarely produces dangerous symptoms. However, it is imperative to establish the existence of hypoglycemia and to distinguish between the two hypoglycemic states. Plasma glucose concentrations must be raised to normal levels as quickly as possible. Clinical improvement should be expected in less than 10 minutes. If there is no improvement after 15 minutes, the initial treatment should be repeated.

Drug Therapies
  • Oral administration of glucose if the patient is awake enough to swallow (10 to 20 g carbohydrate)
  • Intravenous administration of glucose for patients unable to swallow (25 ml of 50% glucose solution)
  • Subcutaneous or intramuscular injection of glucagon (1 mg) is an alternative to the above treatments, but patients must also eat because the effect of glucagon is short.
  • Intravenous mannitol (40 g as a 20% solution over 20 minutes) and glucocorticoids (dexamethasone, 10 mg) may be used to treat a delayed recovery (e.g., patient who remains in a coma after glucose levels return to normal).

Complementary and Alternative Therapies

Alternative therapies may also be useful in regulating blood sugar in the short term.

  • Small frequent meals, preferably five to six a day, high in protein and complex carbohydrates.
  • Minimize simple carbohydrates including sugar, refined foods, juices, and fruit.
  • Eliminate caffeine, alcohol, and tobacco.

Some patients with normal lab values may respond well to dietary changes.

Vitamins and minerals essential to normal glucose regulation include:

  • Chromium picolinate—100 to 200 mcg tid with meals
  • Magnesium—200 mg bid to tid
  • Vanadyl sulfate—10 to 20 mg/day
  • Zinc—15 to 30 mg/day
  • B complex—50 to 100 mg/day
  • Niacinamide—500 mg/day
  • Pyridoxine (B6)—100 mg/day
  • Pantothenic acid (B5)—250 mg/day
  • Vitamin C—1,000 mg bid to tid
  • Vitamin E—400 IU/day


Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites, or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 10 to 20 minutes and drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

  • Siberian ginseng (Eleutherococcus senticosus) provides adrenal support. Use tincture 20 drops bid, or dried extract 100 mg tid for two to three weeks, with a one week rest before resuming.
  • A tincture of equal parts of licorice root (Glycyrrhiza glabra), gotu kola (Centella asiatica), Siberian ginseng, and ginger root (Zingiber officinale), 10 to 15 drops tid, may be used in combination to strengthen the adrenals and alleviate hypoglycemic symptoms.


An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. Constitutional homeopathy can provide overall support, but the underlying cause must be addressed.


May be beneficial in decreasing stress and increasing coping skills.

Patient Monitoring

If a hypoglycemic mechanism is obvious and treatable (or self-limited), then no further diagnostic workup is necessary. If a hypoglycemic mechanism is not apparent, further studies are necessary to determine the cause.

Other Considerations

Diet is one of the most important factors in avoiding hypoglycemic episodes. The diet of choice for hypoglycemia should be low in simple carbohydrates and high in protein and complex carbohydrates. Refined and simple sugars, alcohol, coffee, tobacco, and caffeine-containing soft drinks should be avoided. Avoid fasting, and favor more frequent smaller meals over fewer larger meals. Regular moderate exercise may improve glucose metabolism by increasing insulin sensitivity and glucose tolerance.


Untreated postabsorptive hypoglycemia can result in coma, brain damage, or death.


Patients with reactive hypoglycemia can expect no long-term ill effects because there is no underlying pathology. However, the prognosis for patients with fasting hypoglycemia depends largely on the underlying disease causing the hypoglycemia, which may be progressive and sometimes fatal.


Pregnancy may be a predisposing factor in reactive hypoglycemia and adult-onset diabetes.


Anderson RA, Polansky MM, Bryden NA, Bhathena SJ, Canary JJ. Effects of supplemental chromium on patients with symptoms of reactive hypoglycemia. Metabolism. 1987;36:351-355.

Branch WT Jr. Office Practice of Medicine. 3rd ed. Philadelphia, Pa: WB Saunders Co; 1994:574-575.

Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998:2069-2071.

Mowry DB. The Scientific Validation of Herbal Medicine. New Canaan, Conn: Keats Publishing; 1986:25.

Tyler VE. Herbs of Choice: The Therapeutic Use of Phytomedicinals. Binghamton, NY: Pharmaceutical Products Press; 1994:141.

Wilson JD, Foster DW. Williams Textbook of Endocrinology. 8th ed. Philadelphia, Pa: WB Saunders Co; 1992:1232-1248.

Wyngaarden JB, Smith LH Jr. Cecil Textbook of Medicine. 17th ed. Philadelphia, Pa: WB Saunders Co; 1985:1342-1348.

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.