Charles M. Clark

The Diabetes Education Study: A Controlled Trial of the Effects of Diabetes Patient Education

The Diabetes Education Study (DIABEDS) was a randomized, controlled trial of the effects of patient and physician education. This article describes a systematic education program for diabetes patients and its effects on patient knowledge, skills, self-care behaviors, and relevant physiologic outcomes. The original sample consisted of 532 diabetes patients from the general medicine clinic at an urban medical center. Patients were predominantly elderly, black women with non-insulin-dependent diabetes mellitus of long duration. Patients randomly assigned to experimental groups (N = 263) were offered up to seven modules of patient education. Each content area module contained didactic instruction (lecture, discussion, audio-visual presentation), skill exercises (demonstration, practice, feedback), and behavioral modification techniques (goal setting, contracting, regular follow-up). Two hundred seventy-five patients remained in the study throughout baseline, intervention, and postintervention periods (August 1978 to July 1982). Despite the requirement that patients demonstrate mastery of educational objectives for each module, postintervention assessment 11–14 mo after instruction showed only rare differences between experimental and control patients in diabetes knowledge. However, statistically significant group differences in self-care skills and compliance behaviors were relatively more numerous. Experimental group patients experienced significantly greater reductions in fasting blood glucose (−27.5 mg/dl versus −2.8 mg/dl, P < 0.05) and glycosylated hemoglobin (−0.43% versus + 0.35%, P < 0.05) as compared with control subjects. Patient education also had similar effects on body weight, blood pressure, and serum creatinine. Continued follow-up is planned for DIABEDS patients to determine the longevity of effects and subsequent impact on emergency room visits and hospitalization.

Gestational diabetes: should it be added to the syndrome of insulin resistance?

OBJECTIVE The significance of gestational diabetes mellitus (GDM) results from its short-term detrimental effects on the fetus and its long-term prediction of NIDDM in the mother. We compared several variables associated with insulin resistance between GDM and non-GDM pregnant women to show the similarities between GDM and NIDDM (and thus insulin resistance). RESEARCH DESIGN AND METHODS On the basis of a 3-h oral glucose tolerance test (OGTT), 52 GDM patients and 127 non-GDM patients were recruited from pregnant, non-diabetic women who had a nonfasting 1-h-50-g glucose screening test ≥ 7.2 mmol/l (130 mg/dl) performed between 16 and 33 weeks of gestation (a total of 518 of 3,041 women drawn from six community health care prenatal clinics were screened positive). During the OGTT, several potential markers of insulin resistance were measured at fasting and 2-h time points, in addition to the standard glucose measurements. The relationship of these variables with the diagnosis of GDM was studied. RESULTS GDM patients, compared with non-GDM patients, had 1) higher prepregnancy weight (P = 0.011), prepregnancy BMI (P = 0.006), C-peptide at fasting (P = 0.002) and at 2 h (P < 0.001), insulin at fasting (P = 0.001) and at 2 h (P < 0.001), triglycerides at fasting (P = 0.005) and at 2 h (P = 0.003), free fatty acids at fasting (P = 0.017), β-hydroxybutyrate at fasting (P = 0.007); and 2) lower HDL cholesterol at fasting (P = 0.029). These variables were all predictive of GDM (P < 0.036) individually. Using stepwise logistic regression with all of these variables available, fasting (P = 0.019) and 2-h (P < 0.001) insulin levels, fasting free fatty acids (P = 0.031), and fasting β-hydroxybutyrate (P = 0.036) were statistically significant as jointly predictive of GDM. Comparisons between GDM patients and non-GDM patients matched by BMI confirmed that the metabolic abnormalities persisted when difference in BMI was taken into account. Concomitant blood pressure measurements in women with GDM did not differ significantly from those without GDM. CONCLUSIONS Our results show that many of the known metabolic components of the syndrome of insulin resistance (syndrome X) are predictive of GDM. These results are in keeping with the argument that GDM is one phase of the syndrome of insulin resistance. We suggest that GDM be looked upon as a component of the syndrome of insulin resistance that provides an excellent model for the study and prevention of NIDDM in a relatively young age-group.

How Should We Respond to the Worldwide Diabetes Epidemic

The headlines coming from the International Diabetes Federation meeting in Helsinki this summer were about the worldwide increase in diabetes, particularly affecting the Third World (1). The U.S. will not be spared from this epidemic and its associated personal and societal costs. As the article by Harris et al. (2) clearly documents, there has already been a marked increase in the prevalence of diagnosed and undiagnosed diabetes and impaired glucose tolerance in the U.S., as documented in the sequential National Health and Nutrition Examination Surveys (NHANESs), and particularly in the latest survey (NHANES III, 1988-1994). These data raise two related questions: why are we seeing this increase in prevalence and what does this mean in terms of health costs and outcomes? The explanation that the observed increased prevalence is due to the recent changes in diagnostic criteria or surveillance is adequately refuted by the data presented (2). The increased diabetes prevalence using the new criterion of a fasting blood glucose >125 m^dl and that using the unchanged World Health Organization (WHO) criteria are virtually identical: from 8.9% in 1976-1980 to 12.3% in 1988-1994 using American Diabetes Association criteria and from 11.4 to 14.3% using WHO criteria. Similar increases are seen for impaired glucose tolerance. Thus, the lowering of the level of fasting glucose diagnostic of diabetes did not just reclassify people, rather it identified new cases. Since the survey screens all patients included, ascertainment bias is also quite unlikely. Then, if there are more people with diabetes living at ages 40-74 years, is this due to cohort survival or a higher incidence of diabetes? While not to minimize the true decrease in cardiovascular disease and deaths over the past 20 years, this does not appear to account for the increased prevalence of diabetes. Harris et al. suggest that the increase is due to the increased obesity and sedentary lifestyle seen in the U.S. over the past 20 years (2-4). We share this view, and the worldwide epidemic seems to sustain it. The gene(s) inclining so many members of society to insulin resistance, cardiovascular disease, and diabetes are markedly prevalent in many ethnic groups (5). An improved standard of living seems inevitably to result in lifestyle changes that result in reduced physical activity, increased body weight, and vascular disease and diabetes. It seems almost certain that these lifestyle changes underlie the worldwide increased prevalence of diabetes. Added to this increased prevalence of diabetes is the concomitant increase in the prevalence of impaired glucose tolerance and the newly defined impaired fasting glucose (2). We are struggling with how to address this even larger population known to be at risk for the development of both diabetes and cardiovascular disease. We published data in the June 1997 Diabetes Care documenting the increased cardiovascular risk associated with even mild abnormalities in fasting glucose (6). These observations suggest that the increase in cardiovascular risk occurs at an even lower plasma glucose than does the microvascular risk. Because many of those with impaired glucose at the beginning of a long-term epidemiologic study develop diabetes during the study, it is not certain whether it is the impaired glucose tolerance or the subsequent development of diabetes that is the risk factor for cardiovascular disease. Whatever the explanation, the increased prevalence of all abnormalities in glucose metabolism and of insulin resistance will predictably result in increased cardiovascular disease among these individuals (7,8). How can we address this epidemic? Certainly applying the old and new diabetes therapies is the place to start. But we are hampered in this by our uncertainty regarding the effect of current interventions on either delaying the onset of diabetes or reducing cardiovascular disease (9). Thus, we must pursue a two-pronged attack on the problem of diabetes. First, we must vigorously pursue basic and clinical research into the reasons that diabetes and impaired glucose tolerance are associated with increased cardiovascular risk and how we can prevent the development of cardiovascular disease. We must also examine how to reduce the conversion of impaired glucose tolerance into diabetes. The Diabetes Prevention Program occupies a central role in this latter effort. Second, we must pursue a vigorous public health effort to improve the care of people with diabetes. Diabetes has become a major public health problem that consumes a rising percent of our health care dollars: nearly

Reducing the burden of diabetes: managing cardiovascular disease†

100 billion (one-sixth of all health care costs) and rising at last look (10). How society addresses diabetes as a public health problem will determine the fate of the nearly 18 million diagnosed and undiagnosed in the U.S. and the estimated 200 million people worldwide who will have diabetes as we enter the new millennium (1). The good news is that we have effective treatments likely to improve the lives of people with diabetes and to reduce their long-term complications. The bad news is that these treatments are not being universally applied (11). Effective application of these treatments will require that the public, patients, practitioners, and policy makers take diabetes seriously to ensure that these treatments are effectively and uniformly applied. The recent changes in Medicare reimbursement as part of the budget reconciliation act are an important step. The establishment of the National Diabetes Education Program (NDF.P) is another. Funded jointly by the National Institutes of Health and the Centers for Disease Control, NDEP has brought together over 100 organizations representing a broad cross-section of the public, people with diabetes, health care professionals, payers and policy makers, and industry dedicated to communicating the seriousness of diabetes and the marked difference that treatments can make in human and financial terms. Its public campaigns will be launched in the spring. By working together, we have the opportunity to reduce the potentially devastating effects of the coming diabetes epidemic.

Screening and Treatment of Diabetic Nephropathy by Primary Care Physicians

Of the threats to health and life that beset the person with diabetes, cardiovascular disease (CVD), particularly coronary heart disease (CHD) but also cerebrovascular and peripheral vascular disease, represent the heaviest burden. The relative risk for CVD is very high for Type 1 diabetes, but the absolute risk, in terms of numbers, is much higher for Type 2. In all societies, diabetes increases cardiovascular risk twofold or more, compared with the local non‐diabetic population. Some of the evidence for this diabetes‐related increase in cardiovascular risk is reviewed and its relationship to recognised cardiovascular risk factors considered.

Diabetes and heart disease: An evidence-driven guide to risk factors management in diabetes

ObjectiveTo describe the practices of Indiana primary care physicians related to diabetic nephropathy screening and management.DesignCross-sectional, observational.SettingThe state of Indiana.ParticipantsActive primary care physicians [defined as general internists, family practitioners, and general practitioners) in Indiana who provided care for diabetic patients at the time of the survey (n=1,018)Measurements and Main ResultsPractice patterns relevant to microalbuminuria and overt albuminuria screening and management were assessed along two dimensions: the percentage of patients to whom the practices were applied and the frequency with which the practices were performed. Of 1,141 physicians who responded to the survey, 1,018 were eligible for analysis. Eighty-six percent of physicians reported screening more than half of their patients with type 1 diabetes for overt albuminuria, as did 82% of physicians for their patients with type 2 diabetes. Only 17% of physicians indicated performing microalbuminuria testing on more than half of their type 1 patients. Angiotensin-converting enzyme inhibitor agents were used frequently to treat abnormal urinary albumin excretion when hypertension was present, but less often when hypertension was absent. Physician specialty, year of graduation from medical school, practice location, and familiarity with the results of the Diabetes Control and Complications Trial were significant predictors of screening and treatment practice patterns.ConclusionsPrimary care physicians report practices that allow them to detect overt albuminuria but not microalbuminuria. Angiotensin-converting enzyme inhibitors are frequently used by physicians who test for microalbuminuria, but efforts to increase the detection of early renal damage are needed so that these agents and other therapeutic strategies may be employed at the earliest opportunity.

Demonstration of a Defect in the Formation of Adenosine 3′, 5′-Monophosphate in Vasopressin-resistant Diabetes Insipidus

Type 2 diabetes is a worldwide epidemic. Cardiovascular diseases remain the major cause of death in patients with diabetes, partly because of the association of diabetes and the metabolic syndrome. In this review, we will discuss the evidence for treatment and prevention of cardiovascular diseases in patients with diabetes. Aggressive treatment of hypertension and dyslipidemia is at the cornerstone in the management of heart disease in those patients. Despite its known benefit on the prevention of the microvascular complications of diabetes, intensive glycemic control may or may not have a significant effect on reducing macrovascular diseases. Finally, lifestyle changes and other cardiovascular therapies aimed at preventing heart disease may also prevent or delay the development of diabetes.

Clinical, metabolic and psychological outcomes and treatment costs of a prospective randomized trial based on different educational strategies to improve diabetes care (PRODIACOR).

Extract: Previous studies had indicated that the effects of vasopressin to increase the permeability of collecting ducts to water and to produce a concentrated urine are mediated through adenosine 3′, 5′-monophosphate (cyclic AMP). An investigation was performed to determine whether the lack of response to vasopressin in nephrogenic diabetes insipidus could result from an abnormality in the formation of cyclic AMP. The influence of vasopressin was compared in four water-loaded normal subjects, one patient with vasopressin deficiency, and three patients with nephrogenic diabetes insipidus. Serum and urine osmolality, inulin clearance, and cyclic AMP in urine were determined while 5% dextrose and water was infused at a constant rate before, during, and after administration of vasopressin for 1 hr. Vasopressin given intravenously for 1 hr significantly increased the mean rate of excretion of cyclic AMP in urine from a range of from 1.7 to 3.1 nmol/min before treatment to a range of from 4.7 to 8.9 nmol/min after treatment in the normal subjects and the patient with vasopressin deficiency. There were associated mean increases in urine osmolality from a range of from 39 to 119 mOsm/kg to a range of from 568 to 996 mOsm/kg. In contrast, mean cyclic AMP in urine varied from 0.7 to 1.5 nmol/min and mean urine osmolality varied from 47 to 68 mOsm/kg in the patients with nephrogenic diabetes insipidus and did not change after vasopressin. The findings are interpreted to mean that there is a defect in the adenylate cyclase system in nephrogenic diabetes insipidus. It is not known whether there is an abnormality of the receptor, the enzyme, or both or if there is an associated abnormality of the renal tubules to respond to cyclic AMP.Speculation: The results show that patients with nephrogenic diabetes insipidus do not increase levels of cyclic AMP in urine or concentrate their urine in response to vasopressin. It is proposed that there is a defect in the adenylate cyclase system in these patients which accounts for their lack of response to antidiuretic hormone.

Characterization of Glucose Metabolism in the Isolated Rat Heart During Fetal and Early Neonatal Development

To evaluate the effect of system interventions (formalized data collection and 100% coverage of medications and supplies) combined with physician and/or patient education on therapeutic indicators and costs in Type 2 diabetes.

Role of Lipolytic and Glucocorticoid Hormones in the Development of Diabetic Ketosis

Uptake of 1-14-C glucose, lactate production, 14-C-CO2 production, glycogen content, and the incorporation of 1-14-C glucose into glycogen, protein, and lipid have been studied in isolated fetal and neonatal rat hearts from the sixteenth day of gestation to the fifth neonatal day. The effects of insulin (5,000 μU./ml.) on these processes was also studied. Glucose uptake fell during gestation from 28.4 ± 2.2 to 10.0 ± 1.1 μmoles per gram wet weight tissue per two hours and remained constant after birth. At all ages insulin significantly increased glucose uptake. Lactate production Fell from 77.6 ± 11.5 to 51.5 ± 2.3 μmoles per gram wet weight per two hours between the sixteenth day of gestation and the first day after birth and was not influenced by insulin. Production of 14-C-CO2 from glucose was small (range: 2 to 7 per cent of glucose uptake) and was also unaffected by insulin. Hot KOH extractable cardiac glycogen content rose between the sixteenth and twenty-first day and then fell. The change in hot KOH extractable cardiac glycop; en followed similar changes in 1-14-C glucose incorporation into glycogen. Whereas 1-14-C glucose incorporation into tiot KOH extractable glycogen was unaltered by insulin until after birth, insulin did significantly augment the incorporation of 1-14-C glucose into the cold TCA extractable fraction. This fraction, which includes oligosaccharides destroyed by the hot KOH, also had a higher specific activity than the hot KOH extractable glycogen. The majority of the intracellular counts were in this fraction; the remainder of the counts were in the lactate and acetate or acetoacetate fraction. Insulin did not augment incorporation of 1-14-C glucose into these fractions. Incorporation of 1-14-C glucose into both protein and lipid was less than 2 per cent of glucose uptake and was not influenced by insulin. The data suggest that fetal myocardial development is characterized by a progressive decline in glucose uptake which can be stimulated by insulin from the sixteenth day onward. The conversion of 14-C glucose to 14-C-CO2, protein, and lipid was not influenced by insulin. Incorporation of 1-14-C glucose into hot KOH extractable glycogen was augmented by insulin only after birth under the experimental conditions described. The cold TCA extractable glycogen had a higher specific activity and insulin stimulated the incorporation of 1-14-C glucose into this fraction. It is concluded that insulin augments glucose uptake and incorporation into a glycogen fraction turning over rapidly in the fetal rat heart.