Chapter 161 Diabetes Mellitus
Diabetes is a chronic disorder of carbohydrate, fat, and protein metabolism characterized by fasting elevations of blood glucose levels and a greatly increased risk of cardiovascular disease, renal disease, and neuropathy. Diabetes is divided into two major categories: types 1 and 2. Type 1 diabetes (T1DM) occurs most often in children and adolescents. For this reason it is often referred to as juvenile-onset diabetes. About 5% to 10% of all diabetic patients have T1DM. (Box 161-1 lists the major complications of diabetes.)
BOX 161-1 Major Complications of Diabetes
• Neuropathy: About 60% to 70% of people with diabetes have mild to severe forms of nervous system damage. Severe forms of diabetic nerve disease are a major contributing cause of lower extremity amputations.
• Depression: This is a common accompaniment of diabetes. Clinical depression can often begin to occur even years before diabetes is fully evident. It is difficult to treat in those with poorly controlled diabetes.
T1DM is an autoimmune disease caused by destruction of the beta cells of the pancreas, which manufacture insulin. Positive antibodies against beta cells or insulin occur in 75% of patients with T1DM. Why the immune system is activated to attack the pancreas is not fully clear, but viral infection, food sensitivities, and chemical or free radical damage is likely, combined with genes that may predispose to T1DM. These individuals will require lifelong insulin for the control of blood glucose levels. The individual with T1DM must learn how to manage blood glucose levels on a day-by-day basis, modifying insulin types and dosages as necessary according to meals eaten, liver production of glucose, and the results of regular blood glucose testing.
Type 2 diabetes (T2DM) historically has had an onset after age 40 in overweight individuals but today it is seen even in pediatric patients because of the obesity epidemic, which affects all age groups in America. It is generally thought that up to 90% of all those with diabetes have T2DM. Initially, insulin levels are typically elevated in T2DM, indicating a loss of sensitivity to insulin by the body’s cells. Obesity is a major contributing factor to this loss of insulin sensitivity. Approximately 90% of individuals categorized as having T2DM are obese. The achievement of an ideal body weight in these patients is often associated with the restoration of normal blood glucose levels. Even if T2DM has progressed to the point where insulin deficiency is present, weight loss nearly always results in significant improvements in blood glucose control and dramatic reductions in other health risks, such as cardiovascular disease (Table 161-1).
|Features||Type I||Type 2|
|Age at onset||Usually younger than 40 years||Usually older than 40 years|
|Proportion of all diabetics||<10%||>90%|
|Appearance of symptoms||Rapid||Slow|
|Obesity at onset||Uncommon||Common|
|Insulin levels||Decreased||Normal to high initially, decreased after several years|
|Treatment with insulin||Always||Usually not required|
T2DM is a disease characterized by progressive worsening of glycemic control, which starts with mild alterations in postprandial glucose homeostasis followed by an increase in fasting plasma glucose and often ultimately a lack of production of insulin and the need for insulin therapy.
There are other types of diabetes, such a latent autoimmune diabetes of the adult, sometimes termed type 1.5. This is a slower-onset autoimmune type of diabetes that occurs later in life, often after people reach 35 years of age. Diabetes may also occur as a result of chronic pancreatitis and other insults to the pancreas. Gestational diabetes, another type, affects about 4% of all pregnant women, adding up to about 135,000 cases in the United States each year. This occurs in women who were not diabetic before they became pregnant but developed diabetes during pregnancy. Gestational diabetes occurs more frequently among African Americans, Hispanic/Latino Americans, and American Indians. It is also more common among obese women and women with a family history of diabetes. After pregnancy, 5% to 10% of women with gestational diabetes are found to have T2DM. Women who have had gestational diabetes have a 20% to 50% chance of developing diabetes in the following 5 to 10 years. The least common types of diabetes are genetic disorders, such as neonatal diabetes and mature-onset diabetes of youth, which are generally due to faulty genes causing impaired insulin function.
Prediabetes (also called “impaired glucose tolerance”) is characterized by a fasting glucose between 100 and 125 mg/dL and/or a postprandial glucose of 140 to 199 mg/dL. It is the first step in insulin resistance and estimated to affect 57 million Americans. Many people with prediabetes will go on to develop full-blown T2DM despite the fact that prediabetes is usually reversible and, in most cases, diabetes can be completely avoided through dietary and lifestyle changes. Factors implicated in contributing to prediabetes, insulin resistance, and the progression to T2DM include a diet high in refined carbohydrates, particularly high-fructose corn syrup; an elevated intake of saturated fats; overeating due to increased portion sizes of food; increases in inflammatory markers; lack of exercise; industrial pollution; abdominal weight gain; hormonal imbalances; inadequate sleep; and nutritional deficiencies.
Research increasingly indicates that prediabetes is accompanied by serious health risks, especially an increased risk for cardiovascular disease. Individuals with prediabetes often meet the criteria for the metabolic syndrome (MetS). This is a cluster of factors that together carry a significantly greater risk for cardiovascular disease and the development of T2DM. They include:
By this definition and using data from the National Health and Nutrition Examination Survey (1999-2002), the prevalence of MetS in the United States is 39% among men and women aged 20 and above.1 Among adolescents and using a similar definition, approximately 5.8% meet the established criteria.2 In addition to an elevated risk for cardiovascular disease and diabetes, individuals with MetS report poorer health-related quality of life, both physically and mentally.3
The classic symptoms of T1DM are frequent urination, weight loss, impaired wound healing, infections, and excessive thirst and appetite. Such individuals may suffer from diabetic ketoacidosis upon diagnosis, and they are usually lean in presentation. In T2DM, the symptoms are generally milder and may go unnoticed. For that reason and others, many people with T2DM do not even know that they have the disease. Abdominal weight, fatigue, blurred vision, poor wound healing, periodontal disease, and frequent infections are often manifesting symptoms of T2DM.
The standard method for diagnosing diabetes involves the measurement of blood glucose levels. The initial measurement is generally a fasting blood glucose taken after the patient has avoided food for at least 10 hours but not more than 16. The normal reading is between 70 and 99 mg/dL. If a person has a fasting blood glucose measurement greater than 126 mg/dL (7 mmol/L) on two separate occasions, the diagnosis is diabetes. As mentioned above, a fasting glucose greater than 100 but less than 126 mg/dL is classified as prediabetes.
A postprandial and a random glucose determination are also helpful in diagnosing diabetes. A postprandial measurement is usually made 1 to 2 hours after a meal, whereas a random measurement is one that is made at any time during the day without regard to the time of the last meal. Any reading greater than 200 mg/dL (11 mmol/L) is considered indicative of diabetes (Table 161-2)
|Normal||No elevation > 160 mg/dL (9 mmol/L); <150 mg/dL (8.3 mmol/L) at end of first hour, below 120 mg/dL (6.6 mmol/L) at end of second hour|
|Flat||No variation of more than ± 20 mg/dL (1.1 mmol/L) from fasting value|
|Prediabetic||Blood glucose levels of 140 mg/dL (7.8 mmol/L) to 180 mg/dL (10 mmol/L) at end of second hour|
|Diabetic||>180 mg/dL (10 mmol/L) during first hour, 200 mg/dL (11.1 mmol/L) or higher at end of first hour, 150 mg/dL (8.3 mmol/L) or higher at end of second hour|
A valuable laboratory test for evaluating long-term blood glucose levels is the measurement glycosylated HgbA1c. Proteins that have glucose molecules attached to them (glycosylated peptides) are elevated several-fold in diabetic patients. Normally, about 4.6% to 5.7% of hemoglobin is combined with glucose. An HgbA1c from 5.7% to 6.4% indicates prediabetes. An HgbA1c of 6.5% or higher, particularly when done as a screening test, can diagnose diabetes and is particularly helpful in patients with nondiagnostic fasting blood sugar levels.4 Nonetheless, it is best coupled with a fasting blood glucose measurement and a 2-hour postprandial glucose level for a more accurate diagnosis. Because the average life of a red blood cell (RBC) is 120 days, the HgbA1c assay represents time-averaged values for blood glucose over the preceding 2 to 4 months. An HgbA1c at 5% indicates that the glucose median for the previous 3 months was around 100 mg/dL; for each digit of elevation in the percentage, a rough addition of 35 mg/dL is followed. Thus, an HgbA1c of 7% means that on average over the preceding 3 months the patient’s blood glucose was 170 mg/dL. The HgbA1c index is extremely valuable in providing a simple, useful method for assessing the effectiveness of treatment as well as patient compliance; it should be checked every 3 to 6 months.
In T1DM the insulin-producing cells of the pancreas are ultimately destroyed, in most cases by the body’s own immune system, but what triggers this destruction can vary from one case to another. Genetic factors may predispose a person to damage to the insulin-producing cells through either impaired defense mechanisms, immune system sensitivity, or a defect in tissue regeneration capacity. The entire set of genetic factors linked to T1DM have been termed “susceptibility genes,” because they modify the risk of diabetes but are neither necessary nor sufficient for disease to develop.5 Rather than acting as the primary cause, the genetic predisposition simply sets the stage for the environmental or dietary factor to initiate the destructive process.6 The very term predisposition clearly indicates that something else must occur: less than 10% of those with increased genetic susceptibility for T1DM actually develop the disease.7
In detailed studies, the concordance rate for developing T1DM in identical twins was only 23% in one study8 and 38% in another.9 If one twin develops T1DM after age 24, the concordance rates drops all the way down to 6%, meaning that the other twin is at very low risk for developing the disease. These results and others indicate that in most cases, even where there is a true genetic predisposition, environmental and dietary factors may be more important in determining whether diabetes will develop.10
• There has been a threefold to tenfold increase in the number of people with T1DM throughout the world over the past 40 years. Such a rise simply cannot be explained by an increased number of people genetically predisposed to T1DM. Changes to the human genetic code across large populations take more than one generation.11
• The rate of T1DM can increase dramatically when children in areas where T1DM is relatively rare move to developed countries.12 For example, the rate of T1DM increased by nearly fourfold in one 10-year period in children of Asian origin moving to Great Britain, and the rate increased more than sevenfold in Polynesians migrating to New Zealand.13,14 Genetic factors cannot explain such a rapid change.
Accumulating data indicate that abnormalities of the gut immune system may play a fundamental role in the development of the immune attack on beta cells and the subsequent development of T1DM.15 The intestinal immune system serves a vital role in processing the many food and microbial antigens to protect the body from infection and allergy. What appears to happen in the development of some cases of T1DM is the development of antibodies by the gut immune system that ultimately attack the beta cells. Possibly an underlying factor that may contribute to T1DM is poor protein digestion.
Poorly digested dietary proteins can cross-react with antigens on or within the beta cells of the pancreas. In humans, two proteins that have had the highest degree of incrimination are those found in milk (which contains bovine serum albumin and bovine insulin) and wheat (which contains gluten). For example, dietary bovine insulin differs from human insulin by only three amino acids. If a person develops antibodies to bovine insulin, there is a good chance that these antibodies will also attack their own insulin. In addition to causing antibody-mediated destruction of the beta cells, bovine insulin is able to activate T cells in those predisposed to diabetes in a manner that can also lead to beta-cell destruction by direct attack from T-killer cells.
Strong evidence implicates dietary factors like cow’s milk and gluten as important triggers of the autoimmune process that leads to T1DM. In contrast, breastfeeding has been identified as an important factor in establishing proper intestinal immune function and reducing the risk of T1DM. It is well known that breastfeeding confers a reduction in the risk of food allergies as well as better protection against both bacterial and viral intestinal infections. In case-controlled studies, patients with T1DM were more likely to have been breastfed for less than 3 months and to have been exposed to cow’s milk or solid foods before 4 months of age. A critical review and analysis of all relevant citations in the medical literature indicate that early cow’s milk exposure may increase the risk by about 1.5 times.14,16 In addition, although the risk of diabetes associated with exposure to cow’s milk was first thought to relate only to intake during infancy, additional studies showed that ingestion at any age may increase the risk of T1DM.
There is also considerable evidence that sensitivity to gluten—the major protein component of wheat, rye, and barley—may also play a role. Gluten sensitivity produces celiac disease, another autoimmune disorder. Celiac disease, like T1DM, is associated with abnormalities in intestinal immune function. And as in the case of diabetes, breastfeeding appears to have a preventive effect, whereas the early introduction of cow’s milk is believed to be a major causative factor. The risk of developing T1DM is higher in children with celiac disease. Not surprisingly, the highest level of antibodies to cow’s milk proteins is found in people with celiac disease.17
Population-based studies as well as a prospective study have strengthened the hypothesis that T1DM can be the result of viral infection.18,19 A working theory in this regard is that the immune system becomes slightly confused as to which proteins to attack—the food-based ones such as those from dairy or gluten or the similar proteins on the pancreatic beta cells or insulin. When the person then has a viral infection, the increased stimulation of the immune system is the key that prompts it to become more active, and those confused immune cells begin to damage the pancreas. Gastrointestinal infections due to enteroviruses (e.g., polioviruses, coxsackieviruses, echoviruses) and rotavirus are common, especially in children. All of these viruses replicate in the gut and stimulate the intestinal immune system, which may then activate the insulin-specific immune cells to seek out and destroy beta cells. These viruses and others are also capable of infecting pancreatic beta cells, causing the leukocytes to attack and destroy the beta cells in an attempt to kill the virus. Gastrointestinal viral infections may also increase intestinal permeability and enhance the antibody response to dietary bovine insulin as a result of increased absorption of the intact protein. The severe “leaky gut”—or increased permeability of the small intestine that occurs during and for some time following rotavirus infections (one of the most common causes of acute diarrheal illness in children)—exposes the gut-associated immune cells to large quantities of intact protein.
Cod liver oil may offer significant protection against the development of diabetes because of its high content of vitamin D. The use of cod liver oil became popular during the 1890s to treat rickets, a vitamin D–deficiency disease characterized by an inability to calcify the bone matrix, resulting in softening of the skull bones, bowing of the legs, spinal curvature, and enlarged joints. Beginning in the 1930s, vitamin D was added to milk at a level of 100 IU per 8 oz. As a result, rickets is now uncommon in most developed countries.
Emerging evidence indicates that vitamin D supplementation from cod liver oil and other sources during early childhood can prevent not only rickets but also T1DM.20 In fact, vitamin D fortification may offset some of the “diabetogenic” effect of cow’s milk, but the dosage level in milk may not be sufficient to do so, as the level that was shown to be protective was about 2000 IU—much higher than the amount typically ingested from the consumption of vitamin D–fortified milk.
The most extensive study looking at vitamin D and T1DM enrolled all pregnant women in northern Finland who were due to give birth in 1966 (more than 12,000 women), and their children were then monitored until December 1997.21 Final analysis of 10,366 enrollees demonstrated that children who regularly took vitamin D, primarily from cod liver oil, had an 80% reduced risk of developing T1DM, whereas those who had a vitamin D deficiency actually had a 300% increased risk of developing the disease. One study found that the use of vitamin D from cod liver oil during pregnancy significantly reduced the frequency of T1DM in the offspring.22 Furthermore, studies looking at vitamin D status in the blood of newly diagnosed individuals with T1DM have found much lower levels of the vitamin in these patients than in healthy controls. Because vitamin D can be produced in the body by the action of sunlight on the skin, lack of sun exposure during childhood may also play a role and partially explain the higher T1DM rates in northern countries. Vitamin D in recent research has been shown to prevent autoimmune conditions, including those that attack beta cells, from developing in the body, and observational studies have shown a dose-dependent degree of protection.23
This research indicates that ensuring adequate vitamin D supplementation during pregnancy and early childhood may reduce the risk of T1DM. Vitamin D is important for the normal development of the immune system. In addition, it has been shown that vitamin D inhibits some of the autoimmune reactions that target the beta cells.
In addition to the strong case that can be made for vitamin D as a protective factor, an equally strong case can be made for the benefits of the omega-3 fatty acids in cod liver oil and other fish oils. Human studies have shown that when essential fatty acids (EFAs) are given, the onset of T1DM was significantly reduced. Also, higher levels of n-3 polyunsaturated fatty acids in RBCs have also been associated with reduced risk.24 For one thing, cod liver oil also provides both EPA and DHA, which are vital EFAs in humans. Other studies support the benefit of supplementing EFAs in pregnant women and children. The mechanisms responsible for this effect may be related to improved cell membrane function, leading to enhanced antioxidant status and the reduced formation of inflammatory compounds called cytokines.25
Clear links between increased levels of nitrates (from both dietary sources and water) and an increased rate of T1DM have been established. Nitrates are produced by agricultural runoff from fertilizers and are found in cured or smoked meats such as ham, hot dogs, bacon, and jerky to keep the food from spoiling. Nitrates react within the body to form compounds known as nitrosamines. (Note: The USDA requires all manufacturers of processed meats to add vitamin C to their products to prevent the formation of nitrosamines.) Nitrates and nitrosamines are known to cause diabetes in animals. Infants and young children are believed to be particularly vulnerable to the harmful effects of nitrate exposure.
One of the most alarming features of T1DM is that it is becoming much more prevalent, with a current growth rate of 3% per year worldwide.10 Some areas have been hit particularly hard, such as Finland, Great Britain, Canada, and the United States. Increased nitrate exposure may be a key factor, as the nitrate levels in ground and surface waters of agricultural regions have increased over the past 40 years owing to the use of nitrogen fertilizers. Nitrate contamination occurs in geographic patterns related to the amount of nitrogen contributed by fertilizers, manure, and airborne sources such as automobile and industrial emissions. Nitrate exposure may explain why some geographic pockets have substantially higher rates of T1DM.26,27
Circumstantial evidence from population-based studies also suggests that a higher dietary intake of nitrates from smoked/cured meats is associated with a significantly higher risk for T1DM. These foods severely stress body defense mechanisms and are to be avoided. The habit of feeding children hot dogs, cold cuts, and ham would be a good one for parents to break. Health food stores now carry nitrate-free alternatives to these toxic food choices. Also, investing in a high-quality water purifier is good insurance against ingesting nitrate-contaminated drinking water.
Early intervention in T1DM designed to affect the autoimmune or oxidative process theoretically may be capable of lengthening the “honeymoon” phase or even completely reversing the process. This goal appears to have two candidates: niacinamide and epicatechin.
There are some new data (see, for example, http://www.jdrf.org/index.cfm?page_id=110893) showing that people are now removing gluten and dairy from their diets and are supporting gut health as well as immune system balance.
Niacinamide, also called nicotinamide, has been shown to prevent some of the immune-mediated destruction of the pancreatic beta cells and may actually help to reverse the process.28,29 Observations that niacinamide can prevent the development of T1DM in experimental animals led to several pilot clinical trials that initially confirmed these observations and suggested that if given soon enough at the onset of diabetes, niacinamide could help restore beta cells or at least slow down their destruction. In one of the first pilot studies of people newly diagnosed with T1DM, 7 patients were given 3 g of niacinamide daily and 9 were given a placebo. After 6 months, 5 patients in the niacinamide group and 2 in the placebo group were still not taking insulin and had normal blood glucose and HgbA1c. At 12 months, 3 patients in the niacinamide group but none in the placebo group were in clinical remission.30
The results of this pilot study and others suggest that niacinamide can prevent T1DM from progressing in some patients if given soon enough at the onset of diabetes by helping restore beta cells. As of 2004, there had been 12 studies of niacinamide treatment in recent-onset T1DM or T1DM of less than 5 years’ duration and residual beta-cell mass. Ten of these were double-blind placebo-controlled studies, of which half showed a positive effect compared with placebo in terms of prolonged non–insulin-requiring remission, lower insulin requirements, improved metabolic control, and increased beta-cell function as determined by secretion of a substance known as C-peptide. The main differences between the positive and negative studies in recent-onset T1DM were older age and higher baseline fasting C-peptide in positive studies.31–34
Although some of the studies have shown positive results, it is important to point out that two large studies designed to evaluate the effectiveness of niacinamide in preventing the development of T1DM in high-risk individuals—such as siblings of children who developed T1DM or in individuals who already show elevations in antibodies directed against the beta cells—did not show niacinamide to be effective. The first of these, the German Nicotinamide Intervention Study, did not show much of an effect with 1.2 g of niacinamide daily, while results from the larger study, the European Nicotinamide Diabetes Intervention Trial, did not show benefit with dosages as high as 3 g a day.35,36 A possible shortcoming of these studies was the choice of a timed-released niacinamide. It is possible that such a formulation did provide the peak levels of niacinamide required to block autoimmune mechanisms such as cytokine production.37
In the best-case scenario, niacinamide will likely work for only a few individuals with T1DM of recent onset. Nonetheless, the fact that some patients have had complete reversal of their disease makes a trial of niacinamide worth the effort, especially because there is currently no reasonable alternative.
The dosage recommendation is based on body weight: 25 to 50 mg of niacinamide for every 2.2 lb of body weight or a maximum dosage of 3 g/day in divided doses. Niacinamide is generally well tolerated and without side effects. In fact, no side effects have been reported in clinical trials in T1DM. It does not cause the flushing of skin characterized by high dosages of niacin. However, because it could possibly harm the liver, a blood test for liver enzymes should be performed every 3 months to rule out liver damage.
The second natural compound that may offer benefit is epicatechin. The line of research on its potential role in T1DM of recent onset began with examining the bark of the Malabar kino tree (Pterocarpus marsupium). This botanical medicine has a long history of use in India as a treatment for diabetes. Initially, epicatechin extracted from the bark was shown to prevent beta-cell damage in rats. Further research indicated that both epicatechin and a crude alcohol extract of P. marsupium were actually able to promote the regeneration of functional pancreatic beta cells in diabetic animals.38 Green tea (Camellia sinensis) extract appears to be a better choice than extracts of P. marsupium, as the epicatechin content in a high-quality green tea extract is actually higher than that found in extracts of P. marsupium. Second, green tea extract exerts a broader range of beneficial effects. Green tea polyphenols also exhibit significant antiviral activity against rotavirus and enterovirus—two viruses suspected of causing T1DM.39 Last, green tea extract is considerably easier to find commercially than P. marsupium. Recommended dosages for children below age 6 is 50 to 150 mg; for those 6 to 12 years old, 100 to 200 mg; and for children older than 12 years old and adults, 150 to 300 mg. The green tea extract should have a polyphenol content of 80% and be decaffeinated.
The major risk factor for T2DM is obesity or, more precisely, excess body fat. Approximately 80% to 90% of individuals with T2DM are obese (a body mass index above 30). When adipocytes, particularly those around the abdomen, become full of fat, they secrete a number of biological products (e.g., resistin, leptin, tumor necrosis factor, free fatty acids, cortisol) that dampen the effect of insulin, impair glucose utilization in skeletal muscle, promote glucose production by the liver, and impair insulin release by pancreatic beta cells. Also important is that as the number and size of adipocytes increase, there is a reduction in the secretion of compounds that promote insulin action, including a novel protein produced by fat cells known as adiponectin. (Adiponectin is associated not only with improved insulin sensitivity but also with antiinflammatory activity; moreover, it lowers triglycerides and blocks the development of atherosclerosis, or hardening of the arteries.) The net effect of all these negative actions of fat cells is that they severely stress blood glucose control mechanisms while also leading to the development of the major complication of diabetes: atherosclerosis. Because of all of these newly discovered hormones secreted by adipocytes, many experts now consider the adipose tissue a member of the endocrine system (e.g., the pituitary, adrenals, and thyroid).40,41 Measurements of blood levels of adiponectin and other hormones secreted by fat cells may turn out to be the most meaningful predictors of the likelihood of developing T2DM.42,43
In the early stages of the increased metabolic stress produced by the various secretions of adipocytes and the lack of adiponectin, blood glucose levels remain normal despite insulin resistance because pancreatic beta cells compensate by increasing insulin output. As metabolic stress increases and insulin resistance becomes more significant, the conventional explanation is that eventually the pancreas cannot compensate and elevations in blood glucose levels develop. As the disease progresses from insulin resistance to full-blown diabetes, the pancreas starts to “burn out” and produces less insulin. Under naturopathic care, however, the pancreas can recover just fine and continue to secrete insulin for the rest of the patient’s life. However, with conventional care and especially allowing the patient to eat a high-carbohydrate diet, diabetes is not well controlled and the result is ultimately complete pancreatic failure to produce insulin, thus requiring full use of basal and bolus insulin. It cannot be sufficiently stressed that this scenario is preventable with good diabetes care and if a patient’s HgbA1c remains at 5.7 or less. (See Box 161-2 for risk factors.)
In studies of identical twins, the concordance rate was between 70% and 90% for T2DM. This high concordance points to a strong genetic relationship. Data from family studies also provide additional support, as children with one parent with T2DM have an increased risk of developing diabetes at some point in their lives. If both parents have the disease, the risk in offspring is nearly 40%.44 However, even with the strongest predisposition, diabetes can be avoided in most cases.
The Pima Indians of Arizona have the highest rate of T2DM and obesity anywhere in the world. Research has demonstrated a strong genetic predisposition, but even with this strong tendency it is clear that the high rate of T2DM in this group is related to diet and lifestyle. The Pima Indians living traditionally in Mexico still cultivate corn, beans, and potatoes as their main staples, plus a limited amount of seasonal vegetables and fruits such as zucchini squash, tomatoes, garlic, green pepper, peaches, and apples. The Pimas of Mexico also make heavy use of wild and medicinal plants in their diet. They work hard, have no electricity or running water in their homes, and walk long distances to bring in drinking water or wash their clothes. They use no modern household devices; consequently, food preparation and household chores require extra effort from the women. In contrast, the Pima Indians of Arizona are largely sedentary and follow the dietary practices of typical Americans. The results are astounding. Although roughly 16% of U.S. Native Americans have T2DM, 50% of Arizona Pimas have T2DM and 95% of them are overweight or obese. T2DM is a rarity among the Mexican Pimas and only about 10% can be classified as obese. The average difference in body weight between the Arizona and Mexican Pima men and women was more than 60 lb.45
Further evidence that diet and lifestyle appear to be able to overcome even the strongest genetic predisposition is shown by some of the intervention studies among Pima Indians. When these people were placed on a more traditional diet along with physical exercise, their blood glucose levels improved dramatically and they lost weight. The focus right now, by various medical organizations such as the National Institute of Health, in dealing with the epidemic of diabetes and obesity among the Pima Indians is to educate children on the importance of exercise and dietary choices to reduce diabetes risk.
Other racial and ethnic groups beside Pima Indians that have a higher tendency to develop T2DM include other Native Americans, African Americans, Hispanic Americans, Asian Americans, Australian Aborigines, and Pacific Islanders. It is important for all of these higher-risk groups to learn that when they follow the traditional dietary and lifestyle practices of their original cultures, their rates of diabetes will be extremely low. It appears that these groups are simply highly sensitive to the “Western diet” and lifestyle.
Findings from the U.S. government’s Third National Health and Nutrition Examination Survey (NHANES III) make it clear that diabetes is a disease of diet and lifestyle. Of individuals with T2DM, 69% did not exercise at all or did not engage in regular exercise; 62% ate fewer than five servings of fruits and vegetables per day; 65% consumed more than 30% of their daily calories from fat and more than 10% of total calories from saturated fat; and 82% were either overweight or obese.46
Insights into the independent role of the modern lifestyle versus diet and obesity in the development of T2DM can be gleaned from the Old Order Amish. These 30,000 or so individuals, whose ancestors arrived on U.S. shores in the eighteenth century, maintain religious and cultural beliefs that preclude regular use of modern conveniences such as electrical appliances, telephones, and cars, and they have a physically active lifestyle. By comparison, the 200 million typical Americans living alongside them have, over the past 250 years, willingly adopted the advances of modern technology, making life less physically demanding.
Although the typical Amish diet and rate of obesity do not differ from those of the typical American, the rate of diabetes among the Amish is considerably less—about 50% lower. Although the percentage of Amish with impaired glucose tolerance (prediabetes) is about the same as in other whites in America, apparently not as many Amish go on to develop diabetes. This suggests that physical activity has a protective effect against T2DM independent of obesity or percentage of body fat.47,48
Results from other studies corroborate this hypothesis. Lifestyle changes alone are associated with a 58% reduced risk of developing diabetes among those at high risk because they show evidence of impaired glucose tolerance (as based on results from the Diabetes Prevention Program—a large intervention trial of more than 1000 subjects). The two major goals of the program were a minimum of 7% weight loss/weight maintenance and a minimum of 150 min/week of physical activity similar in intensity to brisk walking.49
Dietary carbohydrates play a central role in the causes, prevention, and treatment of T2DM. In an effort to qualify carbohydrate sources as acceptable or not, two indices have been developed: the glycemic index (GI) and glycemic load (GL). The GI is a numerical value that expresses the rise in blood glucose after a particular food is eaten. The standard value of 100 is based on the rise seen with the ingestion of glucose. The GI ranges from about 20 for fructose and whole barley to about 98 for a baked potato. The insulin response to carbohydrate-containing foods is similar to the rise in blood sugar. The GI is often used as a guideline in dietary recommendations for people with either diabetes or hypoglycemia. In addition, eating foods with a lower GI is associated with a reduced risk for obesity and diabetes.50–52
One of the shortcomings of the GI is that it tells us only about the quality of the carbohydrates, not the quantity. Obviously quantity matters too, but measurement of the GI of a food is not related to portion size. That is where the GL comes into play. The GL takes the GI into account but provides much more accurate information than the GI alone. The GL is calculated by multiplying the amount of carbohydrate in a serving of food by that food’s GI (as compared with glucose) and then dividing it by 100. The higher the GL, the greater the stress on insulin. In Appendix 6, we provide the GI and GL for many common foods.
Research studies are just starting to use the GL as a more sensitive marker for the role of diet in chronic conditions like diabetes and heart disease. The preliminary results are showing an even stronger link in predicting diabetes than the one shown for the GI.50,52 Researchers are also showing that a high-GL diet is also associated with an increased risk for heart disease. For example, when researchers from the Nurse’s Health Study used GL measures to assess the impact of carbohydrate consumption on women, they found that high-GL diets (and, by extension, high-GI foods and greater total carbohydrate intake) correlated with even more significantly greater risk for heart disease than the GI because of lower levels of protective HDL cholesterol and higher triglyceride levels.53 Increased risk for diabetes and heart disease started, on average, at a daily GL of 161. Therefore, we recommend using the information in Appendix 5 to help determine how to prevent the total daily GL from exceeding 150. Keep in mind that the GL is based on the stated serving size; the larger the serving size, the greater the GL.
Population studies as well as clinical and experimental data show diabetes to be one of the diseases most clearly related to an inadequate intake of dietary fiber. Different types of fibers possess different actions. The type of fiber that exerts the most beneficial effects on blood sugar control is the water-soluble form. Included in this class are hemicelluloses, mucilages, gums, and pectins. These types of fiber are capable of slowing down the digestion and absorption of carbohydrates, thereby preventing rapid rises in blood sugar. They are also associated with increasing the sensitivity of tissues to insulin and improving the uptake of glucose by the muscles, liver, and other tissues, thereby preventing a sustained elevation of blood sugar.54,55
Particularly good sources of water-soluble fiber are legumes, oat bran, nuts, seeds, psyllium seed husks, pears, apples, and most vegetables. Large amounts of plant foods must be consumed to obtain adequate levels of dietary fiber, although beans, peas, and legumes are overall the best sources for high fiber intake in relatively easy amounts to ingest. Even the simple change from white flour products to whole-grain versions is associated with a reduced risk for T2DM,56,57 our recommendation is to consume at least 35 g of fiber a day from various food sources, especially vegetables. Fiber supplements can also be taken to achieve greater effects in lowering the GI.
Dietary fat also plays a central role in the likelihood of developing T2DM. Large controlled trials have shown that a reduction of fat intake as part of a healthy lifestyle, combined with weight reduction and exercise, reduces the risk for T2DM. However, more important than the amount of fat in the diet is the type of fat consumed.58 The types of dietary fats linked to T2DM include saturated fats and trans fatty acids (partially hydrogenated vegetable oils) taken in large amounts along with a relative insufficiency of monounsaturated and omega-3 fatty acids.
One of the key reasons why dietary fats appear to be related to the risk for T2DM is that they determine cell membrane composition. That is, a “bad fat” pattern leads to reduced membrane fluidity, which in turn causes reduced insulin binding to receptors on cellular membranes, reduced insulin action, or both. Particularly harmful to cell membrane function are margarine, vegetable oil shortening, and other foods containing trans fatty acids and partially hydrogenated oils. These fatty acids interfere with the body’s ability to use important essential fatty acids (EFAs). One study estimated that by substituting polyunsaturated vegetable oils for margarine containing partially hydrogenated vegetable oil, the likelihood of developing T2DM could be reduced by 40%.59
In contrast to the dampening of insulin sensitivity caused by margarine and saturated fats, clinical studies have shown that monounsaturated fats and omega-3 oils improve insulin action.60 Adding further support is the fact that population studies have also indicated that the frequent consumption of monounsaturated fats such as olive oil, raw or lightly roasted nuts and seeds, nut oils, and omega-3 fatty acids from fish protect against the development of T2DM. Healthy omega-3 fish include wild salmon, trout, sardines, halibut, and herring. All of this evidence indicates that altered cell membrane composition and fluidity play a critical role in the development of T2DM.
One of the most useful food groups to reduce the risk of T2DM is nuts. Studies have shown that consumption of nuts is inversely associated with the risk of T2DM, independent of known risk factors for T2DM including age, obesity, family history of diabetes, physical activity, smoking, and other dietary factors.61 In addition to providing the beneficial monounsaturated and polyunsaturated fats that improve insulin sensitivity, nuts are also rich in fiber and magnesium and have a low GI. Higher intakes of fiber and magnesium and foods with a low GI has been associated with a reduced risk of T2DM in several population-based studies. Eating mostly raw or lightly roasted fresh nuts and seeds rather than commercially roasted and salted nuts and seeds should be advocated.
Cumulative free radical damage leads to cellular aging and is a major factor contributing to T2DM as well as many other chronic degenerative diseases. Several large population-based studies have shown that the higher the intake of fruit and vegetables, the better blood glucose levels are controlled and the lower the risk for T2DM.62 Many factors could explain this inverse correlation. Fruits and vegetables are good sources of fiber and also provide many nutrients and antioxidants. Even something as simple as the regular consumption of salads is associated with a reduced risk for T2DM.63
Studies looking at levels of individualized antioxidants have also shown similar inverse correlations—the higher the level of vitamin C, vitamin E, or carotenes, for example, the lower the risk for T2DM.64–66 Likewise, the lower the levels of antioxidants and higher the levels of fats damaged by free radicals (lipid peroxides), the greater the risk for T2DM.67 In one study, 944 men 42 to 60 years of age were followed closely for 4 years. None of them had diabetes at the beginning of the study. At the end of this time, 45 men had developed diabetes. The researchers found that a low vitamin E concentration was associated with 3.9-fold (390%) increased risk for T2DM in the study subjects.68
One of the hallmark features of T2DM is the presence of higher levels of free radicals and prooxidants,69 particularly an increased production of reactive oxygen species (ROS) and reactive nitrogen species (RNS).70 These compounds are also activated by high blood glucose and elevated levels of saturated fat and, as already mentioned, are produced in the abdominal fat cells of individuals who are overweight or obese.
These compounds greatly stress antioxidant mechanisms, as they directly oxidize and damage cellular components such as DNA, proteins, and cell membrane fatty acids. In addition to their ability to directly inflict damage on these structures, ROS and RNS indirectly induce damage to tissues by activating a number of inflammatory compounds such as nuclear factor-kappa B, which ultimately leads to both insulin resistance and impaired insulin secretion.
Persistent organic pollutants (POPs) include such chemical compounds as polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), hexachlorobenzene (HCB), organophosphates, DDE, and bisphenol A. These compounds have been linked to the development of T2DM. In addition, research indicates that the body load of POPs is not only a significant predictor of T2DM but may also be a more significant risk factor than obesity.71 Those with levels of organochlorine pesticides in the top quartile have an odds ratio of 5.3 for metabolic syndrome.72
Unfortunately, direct measurement of POP levels is difficult and very expensive. However, a good indirect measure is gamma-glutamyltransferase (GGTP). An elevated level of GGTP is a strong predictor of diabetes risk. Those with levels above 40 IU/L have a 20-fold increased risk.73
Several well-designed large trials have shown that lifestyle and dietary modifications can be used to effectively prevent T2DM. That fact has not dissuaded drug companies from sponsoring studies attempting to prevent diabetes with drugs. However, the degree of prevention with drugs pales in comparison with that of diet and lifestyle. For example, in one of the most celebrated studies, 3234 subjects with impaired glucose tolerance (prediabetes) were randomly assigned to be in a group receiving a placebo, the blood glucose–lowering drug metformin (850 mg twice daily), or a lifestyle modification program with the goals of at least a 7% weight loss and at least 150 minutes of physical activity per week. The average follow-up was 2.8 years. The incidence of diabetes was 11, 7.8, and 4.8 cases per 100 person-years in the placebo, metformin, and lifestyle groups, respectively. The lifestyle intervention reduced the incidence of diabetes by 58% and metformin by 31% as compared with placebo. Clearly, the lifestyle intervention was significantly more effective than metformin—a drug with sometimes serious side effects.74
Given the fact that environmental pollutants can increase the risk of developing T2DM, steps can be taken to reduce patients’ exposure to them. This can be done, for example, through the use of organic foods and natural cleaning agents in the home and the avoidance of chemical pesticides. These are all valid steps in preventing environmental toxins undermining the regulation of insulin.
Knowledge and awareness are the greatest allies of people with diabetes. An individual with diabetes who makes a strong commitment to learning about his or her condition and accepts the lead role in a carefully supervised monitoring program that breaks away from the standard recommended by the American Diabetes Association (ADA) greatly improves the likelihood that he or she will lead a long and healthy life. On the other hand, individuals who remain blissfully ignorant about their disease and refuse to undergo regular testing or self-monitoring are far more likely to face years of unnecessary suffering and, more often than not, catastrophic health problems.
Unless it is properly managed and supervised, diabetes can be viewed as a state of biochemical and hormonal anarchy that will lead to organ injury and accelerated aging. Many of the complex control systems that faithfully govern and protect the body are damaged in the diabetic individual. In order for such a person to regain control, he or she must learn how to maintain an intimate awareness of blood sugar, risk factors for atherosclerosis (hardening of the arteries), blood pressure, body mass index, level of fitness, and other factors that determine the risk of developing diabetic complications and experiencing an erosion of his or her quality of life.
Fortunately, diabetic patients who do develop a keen awareness of these risk factors through regular testing and a properly supervised self-monitoring program are also those who are much more likely to benefit from changes in lifestyle: diet, supplements, and, when necessary, medications.
The measurement of glucose in the urine is now entirely passé. Until the mid-1970s, the only option that diabetic patients had to monitor blood glucose was indirectly through urine glucose testing. Normally, the kidneys are able to conserve all of the glucose in the blood that they constantly filter. However, if blood glucose gets too high, the kidneys become unable to conserve all of the glucose, which then begins to appear in the urine. Because the average diabetic patient’s kidneys can completely conserve glucose until the blood glucose reaches about 200 to 250 mg/dL (10 mmol/L), a negative urine glucose reading indicates that the blood glucose since the time of previous voiding has been less than 200 to 250 mg/dL (10 mmol/L). Therefore, the measurement of glucose in the urine is only a crude measurement of blood glucose control and is completely worthless in detecting severe hypo- or hyperglycemia.75 Thus, urinary glucose monitoring is of little value in determining the success of blood glucose control, and it does not provide adequate feedback when lifestyle, diet, or other treatments are adjusted. These days, all diabetic patients should own a glucometer and know how to test their own blood glucose levels.
In any circumstance when the body must derive its primary source of energy from fat, ketones are produced as a by-product. If the level of ketone production is high enough, ketones appear in the urine. In the patient with T1DM or T2DM who cannot produce any innate insulin, ketones appear in the urine when there is a severe deficiency in or activity of insulin. In general this is associated only with T1DM, because the vast majority of patients with T2DM do not develop ketoacidosis. This can occur if a patient with insulin-dependent diabetes accidentally or purposefully forgets to take insulin. It can also occur when such a patient becomes ill or injured or is given high doses of cortisone-related drugs. All of these phenomena may result in a severe loss of insulin effectiveness, resulting in the cells’ inability to take up and use glucose. In such circumstances, blood glucose rises to high levels, high amounts of fat are used by cells that cannot take in glucose, and the blood becomes polluted with toxic levels of acidic ketones. Severe dehydration occurs rapidly because the kidneys are unable to conserve water in the presence of such extraordinary levels of blood glucose. This dangerous state is referred to as diabetic ketoacidosis, and it must be treated as a medical emergency, usually necessitating intravenous insulin, large amounts of intravenous fluids, and careful monitoring, usually in an intensive care unit. Ignoring ketoacidosis can rapidly lead to death.
Because of the events outlined above, the testing of urine or, even better, blood for ketones (using the Precision Xtra glucometer, which can also test for ketones) remains an important part of monitoring only in patients with T1DM who have no remaining pancreatic function. The presence of urine or blood ketones accompanied by high blood sugar readings can be interpreted to determine how far along the ketoacidosis has developed and what type of medical attention is required. For this reason, all patients with T1DM should test their urine for ketones frequently during acute illness or severe stress, especially when blood glucose levels are consistently elevated (>300 mg/dL [16.7 mmol/L]), regularly during pregnancy, or when symptoms suggestive of ketoacidosis such as nausea, vomiting, or abdominal pain are present.
Since its introduction, self-monitoring of blood glucose (SMBG) has revolutionized the management of diabetes.76 The publication of the landmark Diabetes Control and Complications Trial,77 which examined intensive glucose control in people with T1DM, and the United Kingdom Prospective Diabetes Study,78 which examined intensive glucose control in those with T2DM, scientifically proved that the most important factor in determining the long-term risk of serious diabetic complications in both types of diabetes is blood glucose control. Patients who do not maintain vigilant awareness of their blood glucose and who do not make every effort to keep their blood sugar under tight control can expect a significant increase in their risk of serious health problems such as eye, kidney, and heart disease as well as a whole host of other problems including depression, fatigue, impotence, and chronic infections. SMBG is important for a number of reasons:79
• Note that these are whole-blood values that typically run 10 mg/dL (0.6 mmol/L) higher than serum values. To avoid confusing numbers, some home glucose-monitoring kits, even those using whole-blood samples, are now calibrating to serum levels. Check the glucose monitor’s documentation to find out if it is set up to determine whole-blood or serum glucose levels.
Without a doubt all individuals with T1DM must monitor their blood glucose frequently if they want to achieve and maintain good health. In the absence of diabetes, the pancreas monitors blood glucose continuously and adjusts its insulin output depending on moment-by-moment changes. In order to achieve blood glucose levels that are consistently as close to normal as possible, those with T1DM must replicate this natural situation as closely as possible. This means that they must monitor their blood glucose frequently, and they must learn to use this information to make ongoing adjustments to their insulin injections, diet, and exercise.
Intensive insulin therapy allows a diabetic patient to achieve near normal levels of blood glucose along with enjoying improved lifestyle flexibility. With conventional, infrequent insulin injections, the diabetic patient must structure meals and other aspects of lifestyle around his or her injections or face serious abnormalities of blood glucose. On the other hand, with intensive insulin therapy that relies on rapid-acting, short-duration insulin or the use of an insulin pump (an electronic device that provides a continuous injection of short-acting insulins with extra boluses before meals), the timing and size of doses can be adjusted to suit the events of the day.80 Even though it may involve multiple injections (usually before each meal and often at bedtime) and blood glucose measurements up to six times or more each day, intensive insulin therapy results in greater dietary and lifestyle freedom, a higher quality of life and well-being, and near nondiabetic blood glucose control, which is vital for long-term health.
Self-monitoring of blood glucose has an important place in the management of T2DM as well. Each such patient lies somewhere on a spectrum that ranges from mild glucose intolerance (accompanied by insulin resistance and higher-than-normal levels of insulin) to more advanced forms (with more severe insulin resistance, the potential for high levels of blood glucose, ketoacidosis, and partial or nearly complete pancreatic failure with an accompanying lack of insulin). Depending on the severity of the individual’s diabetes, SMBG plays a varying role. Each such patient should own a blood glucose monitor and have become intimately familiar with its use. Even those whose blood glucose is well controlled through diet, lifestyle, and supplements should measure their blood glucose regularly.
Numerous dietary factors, supplements, exercise, stress, and illness can all have a significant impact on blood glucose control. Becoming intimately aware of how all these factors influence diabetes will help motivate these patients to make positive changes and provide immediate feedback as to the success of any changes that have been made.
Those whose disease is more advanced and who have diminished pancreatic insulin production may also benefit from efforts to establish consistently near normal blood glucose control using intensive insulin therapy similar to that of patients with T1DM.81 A C-peptide blood test can provide an estimate of how much insulin a patient is producing and is one way to help determine the appropriateness of using insulin. If T2DM patients are placed on an intensive insulin therapy program, they must perform SMBG as frequently as those with T1DM who are receiving intensive insulin therapy (usually before and 2 hours after each meal).
Many patients with advanced T2DM have diminished insulin production (evidenced by lower-than-normal C-peptide levels). A common way to achieve optimal blood glucose in these individuals is to give one injection of the new, long-acting insulin glargine (Lantus), which provides a smooth, continual release of insulin for 24 hours, along with diet and other medication. Patients on this type of program must measure their blood glucose frequently (usually before and 2 hours after each meal).
Often it is important to know whether a diabetic patient’s pancreas is making insulin, and if so, how much. This assessment can greatly influence treatment, especially in a patient hoping to avoid or cease using injected insulin. The level of pancreatic insulin production can also partially determine the type of medication or natural health products that are more likely to be effective. Once it is known how well the pancreas is producing insulin, the focus may be shifted toward replacing deficiencies in insulin production, stimulating insulin production, preserving pancreatic function, reducing insulin resistance, or a combination of these therapeutic efforts.
One way to determine the level of insulin production is by measuring C-peptide. The pancreas manufactures a large protein called proinsulin first. A piece of this protein (C-peptide) is then snipped off by enzymes, and both C-peptide and the remaining insulin are released into the bloodstream. Injected insulin has no C-peptide, nor does the body ever produce antibodies against it, as it can against insulin. T1DM patients and those who have injected insulin even once are at high risk of having developed insulin antibodies, which can destroy the molecule. The benefits of measuring C-peptide are helpful for both T1DM and T2DM patients, but generally more so for those with T2DM. C-peptide can uncover how much insulin the pancreas is making, which may help to determine how much of a T1DM pancreas is still active. It may even sometimes make it possible, with alternative care, to stabilize the patient’s condition. In T2DM, high C-peptide levels confirm that the patient is highly insulin resistant. If the C-peptide is low, it indicates that the pancreas is so damaged that some type of insulin therapy will be required (Table 161-3).
|Normal||Insulin production at normal level|
|Below normal||Newly diagnosed type 1 diabetic or chronic, long-term type 2 diabetic|
|Above normal||Newly diagnosed type 2 diabetic or a benign pancreatic tumor (insulinoma; rare)|
|Undetectable||Chronic type 1 diabetic or postsurgical removal of pancreas (rare)|
Although diabetic patients must take charge of their illness and be in control of their diet, lifestyle, and glucose monitoring, they are rarely successful without professional guidance. Numerous studies have determined that physician monitoring through laboratory measurements of blood glucose levels can have a major impact on a diabetic patient’s long-term health.
One of the key determinants of blood glucose control is the HgbA1c test (see earlier). Unlike direct measurements of blood glucose, which detect the level at the moment of testing, the HgbA1c test reflects the average level of blood glucose over the preceding 3 months. Studies have shown that the level of HgbA1c closely correlates with the level of risk for diabetic complications. However, an HgbA1c may not be entirely accurate. A patient may have steady, regulated blood sugars that return an HgbA1c of 6%, or he or she may have very high numbers in combination with hypoglycemic events, which can also—because the HgbA1c is an average, median index—show the same HgbA1c of 6%.6 Having an HgbA1c level of less than 5.5% or less is ideal and indicates that blood glucose levels have averaged in a range that is essentially nondiabetic (meaning that the patient is suffering no damage because of his or her glucose level). Owing to the great importance of adequate glucose control, all diabetic patients, should have their HgbA1c levels measured every 3 to 4 months, depending on the stability of their condition. If the HgbA1c number is not clearly known to be the result of good control or fluctuating highs and lows, then a second laboratory test, called Glycomark, is a good one to consider.81a The GlycoMark assay measures blood levels of 1,5-anhydroglucitol. 1,5-AG is found in nearly all foods and is ingested in a regular diet. Once ingested, 1,5-AG is nearly 100% non-metabolized and remains in a relatively constant amount in the blood and tissues. When blood glucose exceeds 180 mg/dL for any period of time, the kidney attempts to reabsorb as much glucose back into the blood as it can. During times of glucosuria, the additional amount of glucose in the kidney blocks 1,5-AG from being reabsorbed into the blood and 1,5-AG is excreted in the urine at a higher rate than normal. Due to the lack of 1,5-AG being reabsorbed, blood levels of 1,5-AG decrease immediately, and continue to decrease until glucose values go below 180 mg/dL. It is this competitive inhibition of 1,5-AG from glucose that allows GlycoMark to accurately reflect any hyperglycemic episodes over 180 mg/dL. The Glycomark test has been shown to be more accurate than an HgbA1c and offers the physician a clearer picture of how well a patient’s glucose levels are being controlled and also shows postprandial spikes more clearly.
Although it is clear that optimal blood glucose control is critical to the health of diabetic patients, several other risk factors must be carefully monitored in all diabetic patients. Early detection of problems through a program of regular screening and monitoring will enable preventive efforts and treatments to be put in place before serious complications or catastrophic problems occur. Table 161-4 provides a checklist for the proper evaluation and monitoring of patients with diabetes.
|Review Management Plan|
|Blood glucose self-monitoring results||X||X|
|Height (for child/adolescent)||X||X|
|Sexual maturation (for child/adolescent)||X||X|
|Skin, including insulin injection sites||X||X|
|Feet: pulses, capillary refill, color, sensation, nails, skin, ulcers||X||X|
|Neurologic: reflexes, proprioception, vibratory sensation, touch (distal temperature sensation, distal pinprick or pressure sensation, standardized monofilament)||X|
|Regular retinal examination||X||X|
|Dilated retinal examination||X|
|Fasting or random plasma glucose (normal/target range: 80-120 mg/dL before meals)||X||X|
|Glycosolated hemoglobin (A1C) (target range: <7% in adults, 7.5 to 8.5, age dependent)||X||X|
|Urinalysis (glucose, ketones, microalbumin, protein, sediment)||X||X|
|Complete Cardiovascular Profile|
|Cholesterol <200 mg/dL||X|
|Triglycerides <200 mg/dL||X|
|Low-density lipoprotein <130 mg/dL||X|
|High-density lipoprotein <35 mg/dL||X|
|Lipoprotein (a) <40 mg/dL||X|
|C-reactive protein <1.69 mg/L||X|
|Fibrinogen <400 mg/L||X|
|Homocysteine <16 µmole/L||X|
|Ferritin 60-200 mcg/L (if elevated, transferrin saturation; if elevated, genetic testing for hemochromatosis only once)||X|
|Lipid peroxides <normal||X|
|Serum creatinine (in adults; in children only if protein is present in urine)||X||X|