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DEFINITION

• The tendency for blood glucose to rise between 4 and 8 AM.
• To be clinically relevant, should have an increase of blood glucose by >10 mg/dl or an increased insulin requirement of 20% during these hours. (Carroll) 

EPIDEMIOLOGY

• Estimates of frequency range from 29-91% in type 1 diabetes (Perriello; Koivisto; Edge; Havlin; Bending; Bolli) , 6-89% in type 2 (Carroll; Atiea; Havlin; Bolli). Overall, about 55% of patients likely experience the dawn phenomenon (Carroll).   
• Mechanism: impaired  insulin sensitivity in muscle and liver from nocturnal secretion of growth hormone. Growth hormone deficient patients do not have the dawn phenomenon. Dawn phenomenon is not inhibited by suppression of cortisol or catecholamines, suggesting that these hormones do not contribute (Edge; Carroll).  
• Poor glucose control is associated with higher magnitude and prevalence of the dawn phenomenon; longer duration of type 1 diabetes has less dawn phenomenon (Perriello); however, in type 2 diabetes, longer duration, with worsening beta cell function, hyperglycemia and need for insulin therapy all contribute to more dawn phenomenon.

DIAGNOSIS

• Blood glucose measurements at bedtime (10-11 pm) and early morning (2, 4 and 8 am) should be obtained. Dawn phenomenon shows an abrupt increase between 4 a.m. and 8 a.m., whereas waning of exogenous insulin effect shows gradual rise between 2 a.m. and 8 a.m. (See Table)
• No currently recognized role for obtaining growth hormone or IGF-1 levels in diagnosis.

SIGNS AND SYMPTOMS

• Signs and symptoms depend on the degree of early morning hyperglycemia.
• The following table illustrates the differentiation of Dawn Phenomenon from waning effect of exogenous insulin. 

Tables/Images

CLINICAL TREATMENT

• The dawn phenomenon contributes to worse glucose control: in one study (Atiea), mean A1c was 9.5% in those with dawn phenomenon versus 8.4% without.
• Treatment may include intensifying insulin therapy to improve overall glycemic control [Perriello G].
• Increasing bedtime basal insulin can be effective unless it causes nocturnal hypoglycemia.
• With insulin pump therapy, increase basal rate by at least 20% specifically in the pre-dawn hours.
• Avoid late night snacking, unless appropriate quick-acting insulin is given.

• Adjust diet content (decrease carbohydrates) and timing of the evening meal so that the glucose level at bedtime is 70-110 mg/dl
• If dietary modification is not enough, consider an intermediate or long-acting sulfonylurea at evening meal.
• Basal insulin is indicated if the dawn phenomenon continues.
• For patients with type 2 diabetes on insulin, treatment similar to type 1 diabetes.

FOLLOW UP

• Continued monitoring of early morning blood glucose levels while therapy is being modified, to assess efficacy and continued need for dietary or pharmacologic adjustments.

EXPERT COMMENTS

• Insulin glargine and detemir, with their slower duration of action,  cause less nocturnal hypoglycemia than NPH insulin.
• Antecedant nocturnal hypoglycemia causing morning hyperglycemia has been called the "Somogyi effect", but evidence suggests that nocturnal hypoglycemia is not a cause of significant morning hyperglycemia (Tordjman).

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