In 1997 the American Diabetes Association changed the diagnosis of diabetes to two fasting plasma glucose (FPG) levels greater than or equal to 126 mg/dL (Table 8-1). The threshold was lowered to 126 mg/dL to better help prevent complications associated with diabetes. Screening for type 2 diabetes is important because of its slow and gradual development, which is often asymptomatic because the body appears to adjust to the increasing BG levels.

Table 8-1

Diagnostic Thresholds for Diabetes and Lesser Degrees of Impaired Glucose Regulation

Fasting Plasma Glucose or 2-hr OGTT
Normal	<100 mg/dL (<5.6 mmol/L) fasting
	<140 mg/dL (<7.8 mmol/L) with 2-hr OGTT
IFG	100-125 mg/dL (5.6-6.9 mmol/L) fasting
IGT	140-199 mg/dL (7.8-11.0 mmol/L) with 2-hr OGTT
Diabetes*	126 mg/dL (7.0 mmol/L) fasting
	200 mg/dL (11.1 mmol/L) with 2-hr OGTT

IFG, Impaired fasting glucose; IGT, impaired glucose tolerance; OGTT, oral glucose tolerance test.

When both tests are performed, IFG or IGT should be diagnosed only if diabetes is not diagnosed by the other test.

^*A diagnosis of diabetes needs to be confirmed on a separate day.

TYPE 1 DIABETES

Type 1 diabetes is generally an autoimmune disease. Simply put, an autoimmune disease occurs when a person’s immune system gets confused and starts attacking itself. In the case of type 1 diabetes the beta cells are attacked by the body’s immune system, with ultimate total destruction of insulin-production capacity. This may be verified by serum laboratory tests for antibodies (the part of the immune system that is mobilized for destruction of perceived foreign invaders in the body).

There are several types of antibodies that are used to indicate type 1 diabetes. The most common test is for the antibody called glutamic acid decarboxylase (GAD antibody). Among middle-age persons, women have been found to have higher GAD antibody levels with more severe loss of beta-cell function than males. Women with high GAD antibodies also tend to have other autoimmune diseases, especially autoimmune thyroid disease (Lindholm, Hallengren, and Agardh, 2004). Evidence of GAD antibodies can take a few years to be detectable after initial symptoms and diagnosis of diabetes (Nagai, Imamura, and Mori, 2005).

The peak age of type 1 diabetes onset is during puberty, but it can occur at any age. Winter months are a peak time of onset of type 1 diabetes. It is believed that the body’s exposure to a viral illness can precipitate the development of the autoimmune process in susceptible individuals. One study found at least one gastrointestinal viral infection in over 80% of the children who later developed antibodies related to the destruction of the beta cells (Salminen and colleagues, 2004). More recently vitamin D deficiency has been linked with increased risk of autoimmune diseases, including type 1 diabetes. This may, in part, explain the increased prevalence of type 1 diabetes among persons of Northern European descent and during the winter months with decreased sun exposure. Minnesota has the highest incidence of type 1 diabetes with its strong population with Scandinavian heritage.

The onset of this type of diabetes is usually sudden and severe. The person with type 1 diabetes has most, if not all, of the clinical signs and symptoms at the time of diagnosis. Type 1 diabetes in very young children tends to be found with severe insulin deficiency at onset. Young age at the onset of diabetes with preceding febrile illness may provoke severe diabetic ketoacidosis or DKA (a condition of excess buildup of ketone bodies from breakdown of body fat as an alternative fuel source). The older the age at onset of type 1 diabetes, the more gradual the development of symptoms. It is now known that persons of any age can develop type 1 diabetes. Therefore it is no longer referred to as “juvenile onset.”

Persons with type 1 diabetes tend to have few relatives with diabetes but do have the genetic predisposition for its development. Persons with type 1 diabetes often have other forms of autoimmune diseases such as thyroid and celiac disease. A study of a population with Northern Italian heritage found 4% with autoimmune thyroid disease and a high prevalence of celiac disease (Spadaccino and colleagues, 2008). A study in Spain found 8% of individuals with type 1 diabetes had celiac disease. However, although a gluten-free diet had no effect on metabolic control of diabetes or growth of children, the increased risk of lymphoma and osteoporosis suggests screening, especially among persons with type 1 diabetes (Nóvoa and colleagues, 2008).

In 1997 the American Diabetes Association proposed two subcategories for type 1 diabetes: type 1A diabetes, with observed autoimmunity, and type 1B, showing no autoimmunity. The latter form of diabetes was found to have variable episodes of insulin deficiency and resulting alterations in insulin requirements with some features of type 2 diabetes (Aguilera and colleagues, 2004). It is perceived in the field of diabetes that there are many variants of diabetes with different classifications and treatments that will one day be better identified.

One subtype of type 1 diabetes is now referred to as latent autoimmune diabetes in adults (LADA). It has been found that in Japan there is a significant number of persons with this form of diabetes. A high level of GAD antibodies predicts the development of insulin deficiency (Kawasaki and Eguchi, 2004). The use of the C-peptide test (see Chapter 5) can rule out LADA. An elevated C-peptide level is found with type 2 diabetes. The more expensive testing for GAD antibodies can be done for those suspected of having LADA who have a low or normal C-peptide level (Bell and Ovalle, 2004). However, to establish a differential diagnosis between type 1 (LADA) and type 2 diabetes in older persons, GAD must be measured (Pfutzner and Kerner, 2005).

Individual differences in detectable autoimmune factors, along with varying levels of insulin sensitivity can make the diagnosis of type 1 versus type 2 diabetes challenging, even for the most experienced endocrinologist (a physician who specializes in the study of hormones). Although most individuals with type 1 diabetes are sensitive to insulin, there are many who also have insulin resistance (Suehiro and colleagues, 2005). In some persons diagnosed with type 2 diabetes, the presence of GAD antibodies has been noted. These individuals had lower fasting insulin levels and had higher high-density–lipoprotein cholesterol (HDL-C) and lower triglyceride levels, such as found with insulin sensitivity and type 1 diabetes (Zinman and colleagues, 2004). With a positive GAD antibody test result, the diagnosis should change to type 1 diabetes.

During the first year after diagnosis of type 1 diabetes, there may be a temporary period of insulin production before the beta cells completely exhaust their production. This is referred to as the honeymoon period. Thus a person with newly diagnosed type 1 diabetes may find that he or she needs little or no insulin after initial treatment of hyperglycemia. Individuals experiencing this should be forewarned that the situation will change as the honeymoon period comes to an end.

Without insulin, life cannot exist. In the days before the discovery of injectable insulin, persons with type 1 diabetes simply wasted away from malnourishment. It is for this reason that type 1 diabetes is an insulin-dependent form of diabetes. Control is accomplished only through insulin injection based on carbohydrate intake and BG levels. Persons taking insulin are best advised to consult with certified diabetes educators (CDEs)—health care professionals who specialize in diabetes management and are required to demonstrate continued proficiency or document continuing education in diabetes. Figure 8-1 shows the basic differences between type 1 and type 2 diabetes.

FIGURE 8-1 Differences between type 1 and type 2 diabetes mellitus.

Cultural Considerations

Eating disorders are fairly common among women with type 1 diabetes. Very neat BG logs of readings from self-monitoring may be an indication that the record was written to “please the doctor” and have fictitious numbers. Hgb A_1c values may contradict the woman’s BG log. Withholding or reducing insulin may be used for weight control. This may be particularly true for women who were raised on strict dietary regimens as advocated before the use of carbohydrate counting. Diplomatic attempts to identify eating disorders are important especially with type 1 diabetes.

TYPE 2 DIABETES

Type 1 diabetes is relatively rare, occurring in about 5% to 10% of all cases of diabetes with the rest being type 2 diabetes. Type 2 diabetes was once referred to as non–insulin-dependent diabetes mellitus (NIDDM) and is chiefly caused by insulin resistance at the cellular level. Type 2 diabetes is no longer correctly referred to as NIDDM because of the confusion surrounding the term. The confusion began when a person with type 2 diabetes started taking insulin. This did not always mean that the person went from having NIDDM to having insulin-dependent diabetes mellitus (IDDM). To prevent further confusion the American Diabetes Association officially dropped the NIDDM versus IDDM classification and generally prefers the numeric designation of type 1 for autoimmune diabetes and type 2 diabetes for all other forms of diabetes.

Increased stress such as with infection, burns, and surgery will raise BG levels, and temporary reliance on injected insulin may be required. Therefore a person with type 2 diabetes may need temporary use of insulin while hospitalized for surgery or during times of illness.

There are varying amounts of insulin production in type 2 diabetes: high, normal, or low. As described previously, it may be that persons with low levels of insulin are slowly evolving into having type 1 diabetes, and they should be screened for antibodies. A person with type 2 diabetes who is underproducing insulin is generally thin and sometimes referred to unofficially as “type 1.” Typically a person with type 2 diabetes actually overproduces insulin and has the associated central obesity found with the metabolic syndrome. It is the insulin resistance at the cellular level that can allow both hyperglycemia and hyperinsulinemia. Heredity plays a critical role in the development of type 2 diabetes. Persons with this form of diabetes generally have many family members with a history of diabetes and the other correlates of the metabolic syndrome. The genetic predisposition and incidence of type 2 diabetes increase in persons whose ancestors are from regions nearer the equator, with the highest prevalence being among persons of African, Native American, Asian, Pacific Island, and Southern European heritage, such as the Hispanic population.

Asian Indians have a high rate of diabetes but low rates of obesity. They do, however, have a high waist-to-hip ratio (WHR) with high levels of insulin resistance and hyperinsulinemia. In a study of Italian persons the combined incidence of diabetes and impaired glucose tolerance (IGT) was over 15% for men and 10% for women. The prevalence was greatest in the regions of central and southern Italy (Pilotto and colleagues, 2004). The known incidence of type 2 diabetes in Spain is about 6%, and the combined rate with IGT, 19% (Martinez and colleagues, 2004). In Greece the overall prevalence of diabetes type 2 was about 8% in men and 6% in women (Panagiotakos and colleagues, 2007).

GESTATIONAL DIABETES

Gestational diabetes mellitus (GDM) is a temporary form of diabetes that occurs during the latter part of pregnancy. It is often found in women with a family history of type 2 diabetes and therefore is generally related to the genetic predisposition to insulin resistance. Because it occurs after fetal development (see Chapter 11), the risk for birth defects is different than for a woman who has type 1 or preexisting type 2 diabetes. There is virtually no difference in pregnancy outcomes for a woman who has GDM or type 1 or type 2 diabetes, as compared with a woman without diabetes, if near-normal BG level is achieved before conception and maintained throughout the pregnancy. See Chapter 11 for diagnostic criteria of GDM.

Increased placental hormones, produced during the latter stages of pregnancy, that work counter to insulin (see the section on counterregulatory hormones) are the primary cause of GDM. Once the placenta has been expelled at the time of delivery, the woman’s BG is likely to normalize. Because GDM is associated with insulin resistance, there is an increased risk of eventually developing type 2 diabetes (refer to Chapter 5 for a review of prevention). A deficiency of zinc and selenium has been noted with GDM or IGT during pregnancy (Bo and colleagues, 2005).

Gestational diabetes mellitus can also be associated with GAD antibodies as found in women with Scandinavian heritage. Arabian women tend to be more insulin resistant than Scandinavian women with GDM, even though the body mass index is the same (Shaat and colleagues, 2004).

WHAT ARE THE SYMPTOMS AND CLINICAL FINDINGS OF DIABETES?

The warning signs of diabetes as they generally occur from moderate to severe hyperglycemia are as follows:

• Abnormal hunger

• Symptoms of hypoglycemia

• Skin disorders

• Infections

• Delayed wound healing

• Unexplained weakness and fatigue

Polyphagia

One of the first symptoms of the development of diabetes is an increased appetite, known as polyphagia. This is the body’s response to the need for energy. However, this need is not being satisfied because glucose is not readily able to enter the body cells and therefore is not able to be adequately used as a fuel source. A health care professional should inquire about a person’s appetite and whether it has changed. Polyphagia may cause weight gain.

Reactive Hypoglycemia

In reactive hypoglycemia, excess carbohydrate causes the body to produce too much insulin. However, because the overproduction of insulin is delayed, the BG level first rises too high and then falls too quickly (Figure 8-2 shows the difference between hyperglycemia and hypoglycemia). This form of glucose intolerance is felt to be a precursor to the development of type 2 diabetes.

FIGURE 8-2 Hyperglycemia and hypoglycemia.

Reactive hypoglycemia is characterized by serum glucose levels in the range of 50 to 60 mg/dL, with symptoms of hypoglycemia (Box 8-1) that are relieved by eating. However, many physicians use the criteria that BG levels need to be below 50 mg/dL to make an official diagnosis. Anyone who experiences symptoms of hypoglycemia will usually note increased, almost ravenous hunger that can lead to overeating and weight gain. Regardless of the official diagnosis, the symptoms need to be taken seriously, and the person needs to be advised on how to prevent them (see medical nutrition therapy [MNT] section below). Only then can serious attempts at weight management be undertaken.

Box 8-1 Common Symptoms That Signal Hypoglycemia

Numbness of the tongue

Double or blurred vision

Persons with hypoglycemia may begin to perspire; they may experience hunger and nervousness; their skin may become pale, cold, and clammy; and they may experience mental confusion, physical tremors, weakness, headache, rapid heartbeat, numbness in the tongue, and double or blurred vision (see Box 8-1). Hypoglycemia also alters mood states. Irritability is well known to occur with the combination of stress and hypoglycemia. Hypoglycemia can result in a severe headache, sometimes referred to as a diabetic headache.

However, not all individuals with diabetes experience these symptoms, especially children, elder adults, and persons who have frequent episodes of hypoglycemia. This is referred to as hypoglycemic unawareness. Hypoglycemic unawareness can be resolved by meticulous prevention of hypoglycemia for at least 2 weeks. The health care professional or close family member should suspect hypoglycemia, and treat it accordingly, when a child with diabetes becomes unusually quiet or fretful or when the older adult with diabetes becomes weak or faint. A physician should be consulted if the cause is not readily apparent or if hypoglycemia occurs frequently.

Acanthosis Nigricans

A skin condition called acanthosis nigricans (see Figure 5-1) is a risk factor for diabetes. In this condition there is a thickening of the skin, usually in the body folds, which takes on a gray, brown, black, or blue pigmentation. Screening for acanthosis nigricans is an easily performed, noninvasive method for identifying adolescents at risk for type 2 diabetes (see Chapter 5).

Teaching Pearl

A good assessment question to ask a patient is whether he or she has to get up in the middle of the night to use the bathroom and how often. Persons with undiagnosed diabetes are often relieved to hear they can again expect an uninterrupted night’s sleep with improved BG control. This can motivate the person to adhere to medical nutrition therapy and exercise prescriptions.

Dehydration

The excess fluid loss associated with high levels of BG and ketones causes water to be taken from body tissues. This can result in dehydration if the water is not replaced and blood glucose controlled.

Dehydration with concentrated amounts of glucose in the blood can cause a condition known as hyperglycemic hyperosmolar nonketotic syndrome (HHNK). This condition used to be commonly found in the elder population, in whom diabetes is much more prevalent and in whom there is a diminished sensation of thirst because of the aging process. Because dehydration of the brain can occur, many elder persons with HHNK have a history of lethargy, sleepiness, and confused state lasting from several days to weeks before progressing into a coma. Dehydration and HHNK are easily treated if caught in the early stages. All older individuals, but especially those with diabetes, should be taught the importance of adequate water intake even when they are not thirsty. Since the use of self-monitoring of BG (SMBG) among the elderly population, HHNK is becoming rare. Medicare covers the supplies for SMBG.

Weight Loss

Because the glucose is staying in the blood or is lost through urination, it is not used for energy, and weight loss can develop. An unintentional rapid weight loss should be assessed to rule out diabetes as the cause. Glucose that does not enter the body cells is excreted in the urine with excess ketones. Both represent wasted energy sources. Weight loss results because the energy demand exceeds available sources. This is more likely to happen with type 1 diabetes or in severe cases of type 2 diabetes in which there is insufficient or no insulin production.

WHAT ARE THE HORMONES INVOLVED IN DIABETES?

INSULIN

Insulin is a hormone that is produced in the beta cells of the islets of Langerhans found in the pancreas; it is produced in response to hyperglycemia. Because insulin is composed of protein, oral intake of insulin is not possible because it would be digested before being used. Inhaled insulin is now available, although it has some limitations in its use (see later section on diabetes medications). Therefore persons taking oral hypoglycemic agents are not taking insulin, but rather are using the medication to help their own natural insulin production work more effectively (such people are diagnosed as having type 2 diabetes because they are producing insulin). Women with gestational diabetes are generally discouraged from using most oral glycemic agents because of potential birth defects.

Insulin allows BG into body cells, where it can be used for energy. The body normally produces small amounts of insulin at all times because it is needed to metabolize carbohydrates for the continual energy necessary to sustain life. This type of background insulin, used in type 1 diabetes management, is referred to as either the “basal insulin” used with insulin pumps (see later section on medications) or the “long-acting” insulin types used with injections. Lantus (generically known as glargine insulin) is increasingly being used as a long-acting insulin (see the following discussion of insulin types and use). The basal insulin is similar to the “background” insulin the pancreas normally makes.

Larger amounts of meal-related insulin are normally produced in the pancreas in relation to carbohydrate intake and resulting rise in BG levels. Internal insulin production works like a thermostat. The BG level rises and insulin is produced; the BG level falls and insulin production mostly stops. Thus “meal bolus insulin,” using short-acting insulins, is now being used in relation to the BG levels as influenced by the carbohydrate content of the meals, whether by insulin pump or by injection with a syringe.

OTHER HORMONES INVOLVED IN DIABETES

Several hormones act in concert to regulate BG levels. Insulin, produced in the pancreas, is the only hormone that lowers BG levels. Many hormones act to raise glucose levels; the most important of these are glucagon, epinephrine (also called adrenaline), cortisol, and growth hormone. These are called counterregulatory hormones because they work in an opposite manner to insulin. Any deviation in the balance of these hormones will cause fluctuations in BG levels.

The Somogyi effect may be noted with an increased production of the counterregulatory hormones in response to hypoglycemia. The implication is that hyperglycemia often follows hypoglycemia. In other words, a low blood glucose level is often followed by high blood glucose level. This effect can be noted with records of SMBG levels (see section below on monitoring) and food/activity. Explaining the Somogyi effect to persons who are on insulin is important because they may try to correct hyperglycemia with more insulin. Taking more insulin starts a roller-coaster effect on BG levels. If the Somogyi effect can be determined, a decreased insulin dose may best stop further hyperglycemia. This is because the underlying cause of hypoglycemia is being corrected and the body will stop producing the excess counterregulatory hormones.

The dawn phenomenon refers to the hormonal changes that occur to wake us up. It is specifically related to increased production of cortisol and growth hormone (both counterregulatory hormones). Because most individuals wake early in the morning, it is called the dawn phenomenon. However, it will occur whenever a person usually wakes up, which is later in the day for evening workers. This phenomenon is seen with SMBG. The consequence is that the morning BG level will rise, even if a person has not eaten. Furthermore, a person with type 2 diabetes or GDM may require smaller amounts of carbohydrates at breakfast to prevent postprandial hyperglycemia. The person with type 1 diabetes may require a higher dose of short-acting insulin in relation to carbohydrate intake at breakfast than at other meals, or those on insulin pumps may require a higher basal rate of insulin in the early morning hours.

Persons taking insulin should be prescribed a glucagon kit that a family member or co-worker can be taught to use if the person with diabetes becomes unconscious from severe hypoglycemia. This kit includes a syringe of sterile water that is injected into a vial containing a glucagon tablet in order to dissolve the tablet and is then drawn back into the syringe for injection in the unconscious person (see section on managing hypoglycemia). Glucagon is a counterregulatory hormone normally produced by the body in response to hypoglycemia.

WHAT ARE MEASURES OF GOOD DIABETES MANAGEMENT?

LABORATORY VALUES

Screening Criteria

Impaired fasting glucose (IFG) (BG level 100 to 125 mg/dL after an overnight fast; see Table 8-1) is now considered diagnostic of prediabetes. The diagnosis of diabetes mellitus requires two FPG (fasting plasma glucose) readings greater than or equal to 126 mg/dL or any BG level greater than 200 mg/dL with signs and symptoms of diabetes. One concern with IFG is that it is not measuring the postprandial rise in BG level. A 2-hour oral glucose tolerance test (OGTT) with 75 g of carbohydrate may be helpful in preventing the complications related to hyperglycemia. IGT is the diagnosis made if the resulting BG level is between 140 and 199 mg/dL after an OGTT. Prediabetes is found with IGT. A value of 200 mg/dL or higher with an OGTT and symptoms indicates diabetes. In one study of those persons who had normal fasting glucose, almost 15% had either IGT or diabetes as determined by an OGTT (Sargeant and colleagues, 2004).

Once the diagnosis is made, the laboratory test called hemoglobin A_1c (Hgb A_1c or now referred to simply as A_1c) should be assessed. Increasingly A_1c is being used as a screening test but is not considered confirmation of the diagnosis of prediabetes or diabetes because uniformity of A_1c testing varies from laboratory to laboratory. For now, it has been suggested that with IFG and an Hgb A_1c value of 6% or higher is indicative of diabetes, and treatment may be appropriate (Jimeno and colleagues, 2004).

Most people know that hemoglobin is a component of the red blood cells used to carry oxygen throughout the body. The A_1c test measures how much glucose has attached to the protein in the hemoglobin (see Figure 8-3 for correlations between Hgb A_1c and average BG level). The A_1c is referred to as a 3-month test, because it measures the average BG level 24 hours a day, 7 days a week, for about 3 months. Because hemoglobin has a lifespan of about 3 months, measuring how much protein has attached to it gives an indication of control over the previous 3 months. The goal is to have the A_1c less than 7% for good diabetes control; the 5% range is normal.

FIGURE 8-3 Hemoglobin A_1c and average blood glucose goals.

It appears that individuals with average fasting glucose level less than 85 mg/dL, A_1c of about 6%, and normal triglyceride levels are significantly less likely to develop diabetes within 5 years than those with average fasting blood glucose level of 100 mg/dL, A_1c near 7%, triglyceride level over 170 mg/dL, and low HDL-C average of 55 mg/dL (Schulze and colleagues, 2008). The need for screening for type 2 diabetes has been noted for children as young as 12 years old (Whitaker, Davis, and Lauer, 2004). Persons with a strong family history of diabetes or those with health problems associated with the metabolic syndrome should be screened earlier. Because the incidence of diabetes increases with age, screening should begin by at least age 50 for all persons.

Monitoring Criteria

Hemoglobin A_1c (A_1c)

Detecting diabetes through screening is only the beginning. Ongoing monitoring of BG level is essential. The glycated proteins or advanced glycosylated end products (AGEs) occur in all body proteins in which glucose is attached permanently and are believed to be a major cause of complications of diabetes. One AGE product that is used is the A_1c test. High BG levels as evidenced by elevated A_1c levels are associated with complications.

Among adolescents and young adults who had type 1 diabetes for 13 years, a mean A_1c level of 8.4% was noted with a prevalence of neuropathy of almost 60%, retinopathy was found in about 1 in 4, and nephropathy in 1 in 20 (Nordwall, Hyllienmark, and Ludvigsson, 2006). The DCCT study set the goal of A_1c less than 7.2%, but increasingly the goal is routinely in the 6% range, or, if there is no risk of hypoglycemia, a 5% range of A_1c to achieve the greatest reduction in diabetes-associated complications.

One problem with attempting to achieve an A_1c in the 5% range for a person using insulin is the likelihood that it is masking chronic episodes of hypoglycemia. Because the A_1c level reflects average BG management, high BG readings can be offset by low BG readings, leading to a desired A_1c number, but not to improved health status because having repeated episodes of hypoglycemia is stressful to the body.

Teaching Pearl

The glycosylation of protein found in body cells can be described as body cells being caramelized.

Among the older population, depending on health status and life expectancy, the target A_1c may be appropriate at a higher level. This is because the potential risk of hypoglycemia and restricted food intake is weighed against the decreased likelihood of complications that take years to develop. For example, Hgb A_1c of 8% indicates an average BG level of about 170 mg/dL, low enough to prevent concerns of dehydration, which may be the chief concern for the frail elder individual.

Self-Monitoring of Blood Glucose

A person with diabetes is generally advised to do self-monitoring of blood glucose (SMBG). With personal BG meters, testing of BG level can be done at home or in other locations, such as at a restaurant or on a football field. Self-monitoring consists of taking a drop of blood and placing it on a strip that is inserted into a BG meter. Several types of meters are available, as are automatic lancet devices. The goals are to keep the BG between 70 and 140 mg/dL or as close as possible, with the higher level for postprandial testing. Having occasional SMBG levels up to 180 mg/dL, although not normal, is considered acceptable.

Although all persons with type 1 diabetes are advised to do SMBG, it is also potentially beneficial with type 2 diabetes. One study of SMBG among persons with type 2 diabetes was associated with decreased diabetes-related morbidity and mortality, and this association remained even among those who were not receiving insulin therapy (S Martin and colleagues, 2006). Use of SMBG can allow a person to recognize direct impacts of types of meals on BG outcomes and plan accordingly. Often by using SMBG to determine carbohydrate tolerance in a person with type 2 diabetes, weight loss will result. However, there appears to be less benefit for persons with non–insulin-treated type 2 diabetes who have A_1c at target (Schütt and colleagues, 2006).

Self-monitoring of blood glucose can be used for monitoring BG levels or determining carbohydrate tolerance or insulin-to-carbohydrate ratio (the amount of insulin required to cover carbohydrate intake—see MNT section below). Recommended times to test BG levels include before meals to help determine insulin doses with type 1 diabetes or 1 to 2 hours postprandially to determine carbohydrate tolerance with type 2 diabetes. This is referred to as pattern management because patterns may be noted that give an indication of when hyperglycemia or hypoglycemia may be predicted based on SMBG and food and activity records.

Typically a meal can be expected to raise the blood glucose level by 50 points (mg/dL). With a fasting blood glucose level of 100 mg/dL, an ideal meal should keep the blood glucose level at about 150 mg/dL approximately 1 to 2 hours after the meal. If the BG level goes higher than this, it indicates either excess carbohydrates in the meal, per individual needs, or a need for increased medication.

The advantage of SMBG is the knowledge and flexibility it affords in diabetes management. Less guesswork is involved, and SMBG allows the person with diabetes greater objectivity in decision making to prevent both hyperglycemia and hypoglycemia.

Testing postprandial BG (PPG) level further promotes A_1c goals. One study found that almost all persons maintaining PPG level of less than 140 mg/dL achieved A_1c of less than 7%, whereas only about two thirds of those achieving fasting BG (FPG) targets of less than 100 mg/dL achieved this target. In the majority of persons, achieving an A_1c of less than 6.2% was related to PPG levels. Control of postprandial hyperglycemia is essential for achieving recommended Hgb A_1c goals (Woerle and colleagues, 2007).

Alternatives to finger sticks for BG monitoring do exist. Increasingly, persons with diabetes are using the forearm to measure glucose levels. A continuous glucose sensor has been developed that works by having a biosensor inserted just below the surface of the skin. Eventually this system will be designed to “talk” with an insulin pump, thus serving as an artificial pancreas. Other devices and means to monitor glucose levels are in the development stage.

Monitoring for detection and treatment of hypoglycemia is another role of SMBG. A BG level of less than 70 mg/dL is indicative of hypoglycemia and should be treated with the 15 : 15 rule, whereby 15 g of quick-acting carbohydrate is consumed, followed by a retest of BG in 15 minutes, and the process is repeated as needed to achieve normal BG level. If the BG level is severely low, less than 50 mg/dL, doubling the carbohydrate to treatment with 30 g of carbohydrate is appropriate. At 15 g of carbohydrate the maximum BG level rise will be 50 mg/dL. If BG level rises more than this, it is due either to the Somogyi effect or excess intake of carbohydrate beyond 15 g.

A person may or may not need a follow-up snack to maintain glucose levels in the normal range after hypoglycemia has been corrected with the 15 : 15 rule. With experience in using SMBG, a person may better gauge the necessity of having a snack. As a general guideline, if the next meal will be several hours later, such as in the middle of the night, it may be beneficial to have a more substantial snack (e.g., half a sandwich) after first correcting hypoglycemia by the 15 : 15 rule. A bedtime snack containing carbohydrates for a person using insulin is advised if the BG level is less than 100 mg/dL.

Teaching Pearl

Questions such as “How do I adjust my diet and insulin for exercise?” or “Can I eat a piece of birthday cake safely?” can be addressed through SMBG. For example, a person might find that a half piece of birthday cake with his or her evening meal may raise the blood glucose level an acceptable amount. If the blood glucose level goes above 200 mg/dL 2 hours after eating the cake, the person might consider eating less the next time.

Fact & Fallacy

FALLACY

Treating hypoglycemia requires adding sugar to a glass of orange juice.

FACT

One-half cup, or 4 oz, of orange juice provides the 15 g of carbohydrate needed to correct hypoglycemia. If sugar is added to orange juice, hyperglycemia is likely to develop. Only if the BG level is less than 50 mg/dL should increased amounts of carbohydrate be used. Each teaspoon of sugar contains 4 g of carbohydrate. The 4 oz of orange juice with an additional tablespoon of sugar equates to 30 g carbohydrate, or an expected rise in BG level of about 100 mg/dL.

Cultural Considerations

Data from the National Health and Nutrition Examination Survey (NHANES) 1999-2002 found about half of adults with previously diagnosed diabetes had A_1c levels less than 7%. Mexican Americans and non-Hispanic African Americans were less likely to achieve good control compared with non-Hispanic whites. This difference did not appear to be due to health care access and use of diabetes treatment (Saydah and colleagues, 2007).

WHAT IS THE MEDICAL NUTRITION THERAPY OF DIABETES?

PREVENTION OF DIABETES

As discussed in Chapter 5, factors found to increase the risk of type 2 diabetes are related to evidence of the metabolic syndrome. Other factors associated with risk for type 2 diabetes include excess weight, physical inactivity, low fiber and high saturated fat and trans fatty acid intake, and either no alcohol or excessive alcohol intake. It is estimated that diabetes can be prevented for the majority of persons at risk with diet and lifestyle changes, including a 5% weight loss for those with excess weight, increased fiber intake, and increased exercise. Following the minimum servings of MyPyramid.gov promotes moderate intake while promoting high nutritional quality and is especially good if they are consumed in several small meals throughout the day. Based on general public health recommendations for diet and exercise, diabetes incidence can be reduced by 58% among persons with prediabetes (Roumen and colleagues, 2008).

There is still some controversy regarding the amount of fat in the diet. A 6-month study with up to 45% fat kilocalories but greater than 20% monounsaturated fat had better impact on FBG levels and insulin levels than a low-fat diet with less than 30% fat kcalories. Keeping saturated fat low was important for achieving these goals (Due and colleagues, 2008).

Vitamin D deficiency has been implicated in the development of both type 1 and type 2 diabetes. This finding resulted in part from recognition of vitamin D receptors in the pancreas. Maintaining normal plasma calcium levels through adequate vitamin D intake is necessary to regulate beta-cell function and insulin production (Palomer and colleagues, 2008). Elevated intracellular calcium level found with primary hyperparathyroidism induces glucose intolerance via insulin resistance (Yamaguchi and Sugimoto, 2006).

A multitude of research has now implicated arsenic toxicity as a causal agent. Insulin resistance and beta-cell dysfunction can be induced by chronic arsenic exposure, which may be responsible for arsenic-induced diabetes mellitus (Tseng, 2004). Many areas in the world have excess arsenic in the water supplies, partly because of mining and agricultural practices.

A low magnesium level, both inside the cell and out, is implicated in the development of diabetes. Magnesium plays a key role in promoting cellular uptake of glucose and regulating insulin action (Barbagallo and Dominguez, 2007). Aside from dietary deficiency of magnesium, there also may be an inherited structural defect in the plasma membranes of cells of individuals who have type 2 diabetes and sodium-sensitive essential hypertension. Abnormal accumulation of saturated fatty acids in cell membranes further inhibits the entrance of magnesium into the cell (Wells, 2008).

Another explanation of low serum magnesium levels has been linked with excess caffeine. This appears primarily true with acute intake of caffeine pills with ultimate impairment in glucose metabolism. Generally, chronic intake of caffeine exclusively from diet has little effect on glucose metabolism (Du and colleagues, 2007).

Uncontrolled celiac disease (refer back to Chapter 4) may have a role in the development of type 1 diabetes. Persons with celiac disease with chronic exposure to gluten have a significantly higher prevalence of anti–islet cell antibodies, found with type 1 diabetes (Verbeke and colleagues, 2004).

Type 2 diabetes and the metabolic syndrome in general have been linked with inflammation. Elevated levels of C-reactive protein may be of particular importance in the development of type 2 diabetes in women (Thorand and colleagues, 2007).

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