[Postgraduate Medicine]
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[SYMPOSIUM]

SYMPOSIUM ON CULTURAL MEDICINE

Diabetes in the Hispanic population

High risk warrants targeted screening and treatment

Manuel Idrogo, MD; Roger Mazze, PhD

VOL 116 / NO 6 / DECEMBER 2004 / POSTGRADUATE MEDICINE

CME learning objectives

  • To recognize signs of prediabetes in Hispanic patients
  • To learn the components of a culturally sensitive diabetes treatment plan for Hispanic patients
  • To become familiar with genetic, environmental, and socioeconomic factors that contribute to diabetes in the Hispanic population

The authors disclose no financial interests in this article and no unlabeled uses of any product mentioned.

Preview: As the Hispanic population in the United States increases, more primary care physicians are being challenged to address the high incidence of diabetes and related metabolic disorders in Hispanic American patients. A variety of genetic, environmental, and socioeconomic factors contribute to this group's high susceptibility to diabetes. In this article, Drs Idrogo and Mazze discuss diagnosis of diabetes in Hispanic patients, as well as culturally sensitive screening and treatment strategies.
Idrogo M, Mazze R. Diabetes in the Hispanic population: high risk warrants targeted screening and treatment. Postgrad Med 2004;116(6):26-36

An estimated 37.3 million people of Hispanic descent live in the United States, constituting about 13.7% of the total population (1-3). The median age of Hispanic Americans (26.6 years) is 10 years younger than that of the general population. Between 5 million and 7.5 million people of Hispanic ancestry may have type 2 diabetes, but less than half of these cases are diagnosed (4-7). The true prevalence and incidence of diabetes among Hispanic Americans are not known, but the estimated incidence of type 2 diabetes in this group is between 200,000 and 400,000 cases per year (8).

Compared to the general US population, a disproportionate number of Hispanic persons (as many as 80% of those with type 2 diabetes and 50% of those at risk for diabetes) have a combination of health conditions, including hypertension, dyslipidemia, obesity, and renal disease, which together are known as metabolic syndrome (9,10). It is estimated that among Hispanic patients with diabetes, 50% of adults and 20% of adolescents had metabolic syndrome before diabetes developed (11).

Genetic and environmental factors leading to obesity and insulin resistance are central to development of diabetes and related metabolic disorders. The Hispanic American population is composed of Mexican, Puerto Rican, Cuban, and other Latin American people who trace their ancestry to a mixture of European, Native American, and African roots (12). These ancestors belonged to agricultural societies, and centuries of subsistence living led to "thrifty genes" that promote obesity, ensuring efficient calorie storage and energy expenditure when food sources are scarce.

In a population with this genetic background, the combination of a sedentary lifestyle and a diet high in fat and refined carbohydrates results in a steady increase in body mass (13). The modern diet of Hispanic Americans tends to be high in refined carbohydrates and saturated fat, such as drinks with a high sugar content and traditional dishes fried in animal oils. Furthermore, meal portions tend to be large. Recent studies suggest that this diet adversely affects adolescents as well as adults: 16% of adolescent Hispanic girls have a body mass index greater than 30 kg/m2 (14).

Prediabetes

When food is plentiful, the same thrifty genes that promote obesity to preserve energy contribute to insulin resistance and, consequently, to hyperglycemia, hypertension, hyperlipidemia, renal dysfunction, and coronary artery disease (15). The relationship between obesity and insulin resistance is well established (16-19). As body mass increases, the amount of endogenous insulin needed to overcome the accompanying insulin resistance increases, until insulin output no longer maintains glucose homeostasis. Patients enter a prediabetes phase of impaired glucose tolerance, characterized by fasting glucose values from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) or glucose values from 140 to 199 mg/dL (7.8 to 11.0 mmol/L) measured 2 hours after a 75-g glucose challenge.

The annual percentage of patients with prediabetes in whom overt type 2 diabetes develops is about 5% in the general US population and may reach 15% in the Hispanic American population. Prediabetes typically develops between the ages of 40 and 60 years in the general US population and between the ages of 20 and 30 years in the Hispanic American population (18).

The number of Hispanic children and adolescents with obesity and prediabetes appears to be increasing (20), possibly because of the high rate of undetected--and thus untreated--hyperglycemia among pregnant Hispanic women. Without treatment, this hyperglycemia can result in infants who are large for their gestational age or macrosomic (21). In pregnancies uncomplicated by hyperglycemia, some insulin resistance may be required to shunt maternal nutrients to the developing fetus. However, in women with abnormally high insulin resistance, overnourishment of the fetus stimulates production of large amounts of fetal insulin, leading to excess production of visceral fat and to organomegaly. Such infants have a body weight above the 90th percentile and a disproportionately high risk of childhood or adolescent obesity and insulin resistance (22), accompanied by increased arterial pressure and elevated levels of triglycerides and very low-density lipoprotein cholesterol (23).

Screening and diagnosis

Regardless of whether the increased risk of diabetes is caused by genetic susceptibility, changes in lifestyle, or hyperglycemia during pregnancy, or a combination of these factors, early identification of patients at risk (through screening) and rapid diagnosis of diabetes and associated metabolic disorders present unique challenges in the Hispanic American population (24). For more than 50 years, screening for diabetes has been primarily based on the incidence of diabetes in a predominantly white population, in which blood glucose levels are the defining characteristic of the disease. In Hispanic populations, earlier and more frequent screening is needed. All persons of Hispanic origin should be screened, independent of age, if they are obese or have acanthosis nigricans or polycystic ovary syndrome. Family history is not a useful predictor of type 2 diabetes in the Hispanic population, because diabetes and prediabetes remain undiagnosed in more than 50% of Hispanic persons with these conditions.

Because large numbers of people in the Hispanic population require diabetes screening, inexpensive laboratory assays are needed. Determination of capillary blood glucose using a reflectance meter under clinic conditions can be an acceptable alternative. If a patient's postprandial (casual) blood glucose reading is greater than 160 mg/dL (8.9 mmol/L), a venous blood sample should be drawn for analysis in a laboratory.

Diagnosis of diabetes generally requires two blood glucose determinations on different days. Fasting values of 126 mg/dL (7.0 mmol/L) or greater and casual values of 200 mg/dL (11.1 mmol/L) or greater are diagnostic of diabetes. Since the conversion rate from prediabetes to frank diabetes is high in Hispanic persons, individuals of any age or weight with a postprandial plasma glucose value greater than 160 mg/dL should be tested annually. For lean Hispanic persons with no signs of insulin resistance, annual screening should begin at 30 years of age.

Although current criteria require the aforementioned blood glucose values for the diagnosis of type 2 diabetes, lower values for the general population, based on preliminary observations about the threshold for complications, are under consideration. Table 1 compares the current criteria with those proposed by the American Diabetes Association.

Treatment of type 2 diabetes is based on whether the patient's underlying impairment is insulin resistance or relative insulin deficiency, or both (25). Because diabetes develops in persons of Hispanic descent at a young age and Hispanic persons tend to be obese, it is likely that insulin resistance is the initial and significant underlying deficiency in this population. In most cases of hyperglycemia, abdominal obesity is sufficient evidence that insulin resistance is present. When there is doubt, insulin levels (total or C peptide) should be measured, since higher-than-normal levels confirm insulin resistance.

In obese patients who have had type 2 diabetes for more than 10 years, beta cell function is likely to be impaired and insulin levels are likely to be below normal. Hispanic persons who are older than 50 years, have a lean body mass, and have had persistent insulin resistance and uncontrolled hyperglycemia are likely to have decreased beta cell function and insulin deficiency. This is true especially when blood glucose concentration is above 350 mg/dL (19.4 mmol/L) and the hemoglobin A1c (HbA1c) level is above 13%.

Treatment

Figure 1 (not shown) presents an algorithm used in the Master DecisionPath treatment protocol developed for the Staged Diabetes Management program at the International Diabetes Center, Minneapolis (26). When insulin resistance is the primary deficiency, whether in children or adults, the therapies of choice concentrate on preserving pancreatic beta cell function while addressing modifiable factors that contribute to insulin resistance (ie, body weight and physical activity). When insulin deficiency is the primary impairment, therapies focus on either facilitating beta cell action or supplementing beta cell insulin production. When both insulin resistance and insulin deficiency are present, the goals of therapy are to "rest" the beta cells, reduce glucose challenge, and control weight.

Medical nutrition and activity therapy
Medical nutrition therapy seeks to replace, reduce, or restrict a patient's caloric intake in order to remove the glucose challenge inherent in high-carbohydrate diets. This approach tends to be more culturally sensitive than diets based on fixed menus or on complete omission of certain foods or drinks. Careful management of carbohydrate intake and increased physical activity help control weight and address excessive glucose challenges and insulin resistance. In general, medical nutrition therapy alone reduces HbA1c by 1% to 2%.

Oral agents
When medical nutrition therapy alone fails to restore normoglycemia, or when the HbA1c value is more than 2% above the normal range (4%-6%), insulin resistance is treated with a combination of pharmacologic agents (insulin sensitizers), such as biguanides and thiazolidinediones, and medical nutrition therapy. Metformin hydrochloride, the most commonly prescribed biguanide, reduces excessive hepatic glucose output, thus improving the fasting plasma glucose level. Its anorexic properties may help produce modest weight loss. Thiazolidinediones enhance insulin activity in target tissue by improving the production and translocation of the glucose transporter isoform GLUT4, which is needed to facilitate the uptake of glucose in insulin-sensitive cells. Metformin and the thiazolidinediones lower blood glucose levels by an average of 60 mg/dL (3.3 mmol/L) and the HbA1c value by 2%.

Insulin deficiency is treated with secretagogues and medical nutrition therapy to lessen the glycemic challenge of foods. Secretagogues, such as sulfonylureas or meglitinide analogues, enhance production of pancreatic insulin by improving the function of the potassium channel in the beta cell. Because of their short half-life, meglitinide analogues can be taken just before a meal to increase postprandial insulin production. Secretagogues generally reduce HbA1c by 2%.

Treatment with a combination of a sensitizer and a secretagogue has an additive effect, lowering blood glucose levels by as much as 90 mg/dL (5 mmol/L) and the HbA1c value by 3%.

Alpha-glucosidase inhibitors, a third class of oral agents, can be used to block the rapid breakdown and absorption of carbohydrates, particularly in the early phases of diabetes, when changes in a patient's dietary composition are critical. The effectiveness of these inhibitors is limited to less than a 1% reduction in HbA1c level. Because patients may change their diet to avoid the gastrointestinal side effects of these drugs, the inhibitors are often used as behavior modifiers.

When blood glucose levels are greater than 300 mg/dL (16.7 mmol/L) or the HbA1c concentration is above 11%, combinations of oral medications fail to lower blood glucose values to within the normal range. At this level of glycemia, insulin is the most effective therapy.

Insulin
Insulin therapy should be initiated when oral agents fail to restore euglycemia in patients with either primary insulin resistance or insulin deficiency. By lessening the body's reliance on endogenous insulin and enhancing glucose uptake in target tissue, exogenous insulin lowers blood glucose levels, thus allowing the beta cells to rest.

Combination oral agent and insulin stage: Patients who have been treated with oral agents but need insulin may begin therapy with long-acting insulin (0.1 U/kg) at bedtime while maintaining the oral treatment. The oral agent may then be slowly replaced by additional injections of insulin. This allows the patient to adjust to the insulin therapy while the physician addresses typical concerns.

Because obesity is a major concern for Hispanic patients with diabetes, it is very important that caloric intake be controlled when insulin is initiated. Total calories should remain unchanged but be redistributed among meals and snacks to offset the initial hypoglycemic effect of insulin. Body weight usually increases slightly with improved glycemic control because the calories consumed are used rather than expelled. Once euglycemia is restored, the physician and patient can again address decreasing the patient's caloric intake.

Gradual introduction of long-acting insulin at low doses reduces the risk of hypoglycemia. Careful and slow titration during the introduction of rapid-acting insulin should further reduce the risk of hypoglycemia.

Insulin stages 2 and 3: Stages 2 and 3 in figure 1 (not shown) represent conventional treatment regimens that rely on patients to follow a rigid meal and physical activity plan. The success of these steps depends on consistent action curves of regular insulin or a rapid-acting insulin analogue combined with use of intermediate-acting insulin (NPH). These therapies require fewer injections than physiologic insulin therapy but necessitate use of about 20% more insulin and present a greater risk of midafternoon or overnight hypoglycemia.

Insulin stage 4: Insulin therapy should mimic the normal physiology of fasting and meal-related insulin requirements. A long-acting insulin (eg, glargine) should be used to meet basal insulin requirements, and bolus injections of regular insulin or a rapid-acting insulin analogue can supply meal-related requirements.

If insulin is initiated at diagnosis, a patient's total daily insulin dose should start at 0.3 U/kg, 50% of which should be given in an injection of glargine at bedtime (or in the morning). Alternatively, when there is no medical emergency (risk of hyperglycemic hyperosmolar syndrome), insulin therapy can be initiated with a single injection of glargine (0.1 U/kg) at bedtime. This dose is then adjusted upward to a maximum of 0.4 U/kg or until the fasting blood glucose concentration is less than 100 mg/dL (5.6 mmol/L), whichever is achieved first.

In the next step, the patient uses self-monitored blood glucose values to identify the meal that consistently causes the highest postprandial blood glucose excursions. An injection of a rapid-acting insulin analogue is administered before this meal (in an initial dose of 0.1 U/kg, which is then adjusted upward to 0.3 U/kg or until the postprandial blood glucose level reaches 140 mg/dL [7.8 mmol/L]). Injections of rapid-acting insulin may be needed before other meals, depending on the patient's self-monitored blood glucose values. Generally, this approach results in 50% of insulin being administered as basal injections and 50% as bolus injections (total daily dose, 1 to 1.5 U/kg).

Children and adolescents

Although Hispanic children and adolescents have a high incidence of prediabetes and type 2 diabetes, it should not be assumed that they have type 2 diabetes if hyperglycemia is discovered, even if they are obese. The possibility of type 1 diabetes needs to be addressed as well. Additionally, Hispanic children and adolescents should be evaluated for metabolic syndrome (table 2).

The pharmacologic agents used to treat adults may not be appropriate for children with type 2 diabetes. Medical nutrition and activity therapy is the first treatment choice when the fasting blood glucose level is less than 200 mg/dL (11.1 mmol/L) and the postprandial blood glucose level is less than 250 mg/dL (13.9 mmol/L). When the blood glucose concentration is elevated but the HbA1c value is 11% or lower, metformin can be used. However, because metformin passes the placental barrier, adolescent girls who engage in unprotected sexual intercourse should receive insulin. Insulin therapy should be initiated if the HbA1c value is above 11%, using the same treatment approach as that used in adults.

Patient education and self-care

Teaching patients to self-monitor their blood glucose, recognize hypoglycemia, plan their meals, exercise regularly, and observe and report complications is a central component of diabetes care. Hispanic patients require culturally sensitive approaches, including written materials provided at an appropriate reading level and in the language with which they are most comfortable.

Conclusion

The enormous variety of available pharmacologic and other therapies can lead to substantial confusion about diabetes management in the primary care setting. This is especially true for minority patients, whose socioeconomic circumstances may complicate treatment choices. Hispanic persons, perhaps more than members of any other minority group, are highly susceptible to hyperglycemia accompanied by metabolic syndrome. Each encounter to monitor diabetes should be seen as an opportunity to screen for hypertension, dyslipidemia, and renal disease. A patient with metabolic syndrome should be considered at high risk for diabetes.

The high birth rates, relative youth, and high immigration rates of the Hispanic population are contributing factors in the growing number of people with diabetes in the United States. Because diabetes develops earlier in this population, the needs of children and adolescents (who traditionally are not screened for type 2 diabetes) must be accommodated.

The nation's healthcare delivery system is not yet equipped to meet the added demand for diabetes prevention, screening, treatment, and education services. Hispanic Americans, who are likely to reside in urban areas and depend on public health facilities, face special socioeconomic, language, cultural, and educational challenges when seeking healthcare. These factors present additional obstacles to care, underscoring the imperative of the US healthcare system to organize its services to meet the specific health needs of the Hispanic population.

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Dr Idrogo is assistant professor of family medicine and Dr Mazze is clinical professor of family medicine, department of family medicine, University of Minnesota Medical School--Twin Cities. In addition, Dr Idrogo is WHO Chief Primary Care Officer, International Diabetes Center, Minneapolis. Dr Mazze is also Chief Academic Officer, International Diabetes Center. Correspondence: Manuel Idrogo, MD, University of Minnesota/St Joseph's Hospital Family Medicine Residency Program, 580 Rice St, St Paul, MN 55103. E-mail: idrog001@umn.edu.

Symposium Index

Mexican Americans have the highest overall prevalence of metabolic syndrome. To learn more about this condition, go to the Foldout Feature.

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