Background Research

"Diabetes mellitus (DM) is a common endocrine disorder. It is estimated that approximately 16 million Americans are afflicted with the disease—a number that is projected to double by 2010. Twenty percent of U.S. citizens over 60 have DM.114. An estimated 5.4 million of the 16 million do not realize they have the disease. This is unfortunate, since early and continued treatment helps prevent some of the disastrous consequences of DM. These consequences can range from blindness, to amputations of limbs, periodontal disease, renal failure, hypertension, neuropathy, cardiovascular disease and a great reduction in the quality of life. African Americans, Hispanics and American Indians are especially susceptible to diabetes."

Harris, NO &  Hicks, JL. Chapter 22: Preventive dentistry in a hospital setting, in Primary Preventive Dentistry, 6th ed., 2004.Available on STAT!Ref.

2. Genetics or pathophysiology  What genetic or physiolologic mechanism leads to the conditon’s symptomology?  

“Appearance of the IDDM phenotype is thought to require a predisposing genetic background and interaction with other environmental factors. Rotter and Rimoin (1978) hypothesized that there are at least 2 forms of IDDM: a B8 (DR3)-associated form characterized by pancreatic autoimmunity, and a B15-associated form characterized by antibody response to exogenous insulin.”

National Center for Biotechnology Information.  Online Mendelian Inheritance in Man. Diabetes mellitus, insulin-dependent:  Clinical features.   http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=222100.  Accessed 9/24/07.

3. Clinical Picture What are the signs and symptoms of this condition? What are some common complications?

Increased urination is a consequence of osmotic diuresis secondary to sustained hyperglycemia. This results in a loss of glucose as well as free water and electrolytes in the urine. Thirst is a consequence of the hyperosmolar state, as is blurred vision, which often develops as the lenses are exposed to hyperosmolar fluids.
Weight loss despite normal or increased appetite is a common feature of type 1 when it develops subacutely. The weight loss is initially due to depletion of water, glycogen, and triglycerides; thereafter, reduced muscle mass occurs as amino acids are diverted to form glucose and ketone bodies.
Lowered plasma volume produces symptoms of postural hypotension. Total body potassium loss and the general catabolism of muscle protein contribute to the weakness.
Paresthesias may be present at the time of diagnosis, particularly when the onset is subacute. They reflect a temporary dysfunction of peripheral sensory nerves, which clears as insulin replacement restores glycemic levels closer to normal, suggesting neurotoxicity from sustained hyperglycemia.
When absolute insulin deficiency is of acute onset, the above symptoms develop abruptly. Ketoacidosis exacerbates the dehydration and hyperosmolality by producing anorexia and nausea and vomiting, interfering with oral fluid replacement.
The patient's level of consciousness can vary depending on the degree of hyperosmolality. When insulin deficiency develops relatively slowly and sufficient water intake is maintained, patients remain relatively alert and physical findings may be minimal. When vomiting occurs in response to worsening ketoacidosis, dehydration progresses and compensatory mechanisms become inadequate to keep serum osmolality below 320-330 mosm/L. Under these circumstances, stupor or even coma may occur. The fruity breath odor of acetone further suggests the diagnosis of diabetic ketoacidosis.
Hypotension in the recumbent position is a serious prognostic sign. Loss of subcutaneous fat and muscle wasting are features of more slowly developing insulin deficiency. In occasional patients with slow, insidious onset of insulin deficiency, subcutaneous fat may be considerably depleted.”

Masharani, U.  Diabetes mellitus and hypoglycemia: Signs & symptoms: Type I diabetes,  in SJ McPhee et al.   Current Medical Diagnosis and Treatment, 46th ed., 2007. Available on STAT!Ref.

4. Diagnosis  What diagnostic tests or procedures are commonly employed for this condition?

“If the patient is in a state of diabetic ketoacidosis or is symptomatic from marked hyperglycemia, the degree of hyperglycemia, the acid-base status, electrolytes, and the presence of acetone are urgently assessed. For the nonacute situation, at the patient's first visit, the minimum tests required are a complete urinalysis and determinations of blood glucose and HbA1c. It is now usual to add to these a chemistry panel that includes measurements of lipids, liver and kidney function, and electrolytes and a complete blood count.”

Ramachandiran Cooppan.  General approach to the treatment of diabetes mellitus:  Laboratory studies, in Joslin's Diabetes Mellitus, 14th ed., 2005. Available on Books@Ovid. 

5. Therapeutics What is the common medication or treatment for this condition?

“ Use insulin as the cornerstone of drug therapy for type 1 diabetes.  Set a target for glycemic control based on the patient's risk of hypoglycemia and underlying medical conditions.  Note that unless contraindicated, the primary treatment goal is to achieve HbA1c <7%.

  • Intervene and consider changing therapy if HbA1c >8%.
  • Consider the following conditions as contraindications to tight control:
    ◊ History of unconcious reactions
    ◊ Hypoglycemic unawareness
    ◊ Seizure disorder
    ◊ Clinically apparent cardiovascular or cerebrovascular disease."

Diabetes Mellitus, Type 1.  American College of Physicians PIER.  Available on STAT!Ref.

6. Dental management  What concerns do these patients present in the dental chair?  Are there any drug-drug interactions to consider for this condition?  Is there a bidirectional relationship between the condition of interest and a dental problem?

"Theoretically, there is a basis for either a decreased or increased caries prevalence for Type 1 diabetics. Normally, if there is a good self-care (with an effective mechanical and chemical plaque control regimen), there is a lower count of cariogenic organisms and a lower DMFS. If there is a diet with minimum carbohydrate there is a lower caries incidence. Another moderator is the flow of saliva, with an inverse relationship between flow rate and caries development. A look at several studies is necessary to determine what factor(s) are most determinant for the caries.
Twetman et al. after a three year study with adolescents of 8-15 years of age, concluded that the main most influencial determinants for high caries development over the period of the study were metabolic control, poor oral hygiene, previous caries experience and high levels of lactobacilli. Also there was a higher glucose in the resting saliva."

"If there is a relationship between the level of blood serum glucose and periodontitis, then a high glucose level for an individual should have a significant parallel high CPITN score. There are two studies that verify this assumption.
A large-scale study involving 10,590 subjects in Israel charted abnormal blood glucose (levels over 120 ml/dl) with elevated CPITN scores of above 4.5.117 In the second smaller study of 40 subjects—20 with diabetes, and 20 control subjects. It was found that there was a steady increase in blood serum glucose (142-173 mg/dl) that paralleled that of an increasing CPITN score (13.5-19.1)."

" In reviewing the literature, there is a consensus that periodontal disease has an adverse effect on the severity of DM, and vice versa that the severity of DM has an adverse effect on the severity of periodontal disease—a bi-directional relationship (Figure 22-9). The bi-directional etiology signals the need for cooperation between the medical and dental professions, as echoed in the following statements.
Statement: Poorly controlled diabetics have a greater incidence of severe periodontal disease compared with those patients who are well controlled or have no diabetes mellitus."

      Harris, NO &  Hicks, JL.Chapter 22. Preventive dentistry in a hospital setting: caries; the relationship of diabetes mellitus to the CPITN; and periodontal disease and diabetes mellitus—bi-directional diseases, in Primary Preventive Dentistry,  6th ed., 2004.  Available on STAT!Ref.

7. Public-health policy  What government agency provides information or  programs addressing this condition?

National Library of Medicine.

MedlinePlus. Diabetes: Health topic. http://www.nlm.nih.gov/medlineplus/diabetes.html. Accessed 9/24/07.

EBM Question

What is the effect of ____low-glycemic diet________________(intervention)
on _________ glycemic control (reduced HbA1c levels)________(outcome)
for _________adults with Diabetes (Type 1)_______________ (specific group of patients)?

Citation to the Best Evidence

Brand-Miller J. Hayne S. Petocz P. Colagiuri S. Low-glycemic index diets in the management of diabetes: a meta-analysis of randomized controlled trials. Diabetes Care. 26(8):2261-7, 2003 Aug.

Summary of the Evidence

The study I cite above is a meta-analysis. 

"Choosing low-GI foods in place of conventional or high-GI foods has a small but clinically useful effect on medium-term glycemic control in patients with diabetes. The incremental benefit is similar to that offered by pharmacological agents that also target postprandial hyperglycemia."

Implications for Practice

I have reservations about this study because it states: "Many of the studies included in the meta-analysis involved only small numbers of subjects and were of short duration."

The author, however, goes on to say: " Nonetheless, the findings suggest that there are clinically useful benefits of using low-GI diets in the management of diabetes, over and above those produced by conventional or high-GI diets. After an average duration of 10 weeks, subjects with type 1 and type 2 diabetes who were following low-GI diets had HbA1c levels ~0.4% points (CI 0.1-0.7) lower than those ingesting a high-GI diet."

So I conclude that this diet would be beneficial for my patient.