We start each month with headlines, short up-dates on what we find in journals, newspapers, etc. Then we will present abstracts. This month we will present articles on the impact of diabetes on mortality in diabetic patients with MI, diet, growth and risk of type 1 diabetes and depressive symptoms, insulin resistance and risk for diabetes in women.
November 7th brought the news that the National Diabetes Action Plan was announced by HHS Secretary Thompson which made the commitment to reverse the epidemic of diabetes in the United States. The Plan provides recommendations for individuals, families, health care providers, government officials, employers, as well as members of the media to get them to address diabetes, which as we all know is a growing health problem.
The Nov.24the issue of JAMA had an article which studied low-glycemic diets and low fat diets. Mark A. Pereira et al compared a diet rich in low-glycemic carbohydrates- the type that stabilizes blood sugar with a conventional low-fat diet that included carbohydrates with a high glycemic index. In the study, those on the low-glycemic diets reduced the risk factors for heart disease and diabetes and improved blood pressure and body fats. Those on this low-glycemic diet got 43% of calories from carbohydrates, 27% from protein, and 30 % from fat. Both groups lost the amount of weight, but those on the low-glycemic diet reported less hunger and their resting metabolic rate dropped less. This drop usually occurs during diets.
Northwestern University School of Medicine in Chicago found that the annual Medicare charges for severely obese men were $6,192 more per year than for non-weight men-84% higher. For severely obese women the annual charges were $5,618 more per year, or 88% higher than for women who were not overweight. The article in JAMA states that younger Americans who are overweight today are threatening to hit the U.S. government’s Medicare system with much of this cost. About 12% of US citizens aged 65 and older are currently considered obese. This figure is likely to increase 20% by 2050.
Over the years we have suggested that you test your blood glucose levels after you eat not just in the morning when you rise or before meals. Here is a good reason to do so. The Archives if Internal Medicine 2004;164:2090-2095 had an article on Postprandial glucose regulation and diabetic complications by Antonio Ceriello, MD et al. It is a known fact that atherosclerotic disease accounts for increased mortality and morbidity associated with type 2 diabetes. This review of the research brings us research that shows that postprandial glycemic control is a better predictor for diabetic complication than fasting glucose levels or HbA1c levels. They hypothesize that postprandial glucose may have a direct toxic effect on the vascular endothelium, mediated by oxidative stress that is independent of other cardiovascular risk factors such as hyperlipidemia. Postprandial hyperglycemia may assert effects thorough its substantial contribution to total glycemic exposure. All in all, please ask your health care team to show you how to vary the times you take your glucose levels so that you know how you fare after you eat and how soon your glucose levels come back to normal. There are known ranges that your physician will know about to help you.
Diabetes Care 27:27:2936-2941,2004 has an article titled Sympathetic and parasympathetic neuropathy are frequent in both type 1 and thpe2 diabetic patients by Carolin Freccero, MD et al. The researchers examined the frequency of sympathetic verses parasympathetic neuropathy in type 1 and type 2 diabetic patients. They examined 43 patients with type 1 diabetes and 17 with type 2. The researchers found that both neuropathies were frequent in both type 1 and type 2 diabetic patients. However, there was a difference between the two types of diabetes. Sympathetic and parasympathetic nerve functions correlated in type 1 but not in type 2 diabetic patients. The explanation for this discrepancy might be that parasympathetic nerve function was most severely affected among type 2 diabetic patients.
Finally, good news from Clinical Diabetes 22:157-158, 2004 which shares a landmark study “Polypill" for cardiovascular disease prevention by K.M. Venkat Narayan, MD, MPH, FRCP, FACP. The polypill is composed of a statin, three pressure-lowering drugs, each at half dose, aspirin, 75mg, and folic acid, 0.8 mg. One-third of those taking this polypill from age 55 years or from diagnosis of diabetes or CVD would potentially benefit, gaining on average 11 years of life free from ischemic heart disease or stroke. Such a polypill would cause adverse symptoms in 8-15% of those taking it, depending on specific components in the formulation. The researchers concluded that the polypill if taken by everyone (without contraindications) aged 55 and older and everyone with existing CVD or diabetes regardless of their age could prevent ischemic heart disease and stroke.
Now we bring you the Abstracts that we promised. The Archives of Internal Medicine 2004;164:2273-2279 has an article titled Impact of diabetes on mortality in patients with myocardial infarction and left ventricular dysfunction by Alvaro M. Murcia, M.D. et al. Diabetes is a major risk factor for developing heart disease. In patients who survive myocardial infarction, less is known about subsequent morbidity and mortality. The researchers evaluated the effects of diabetes in post-MI with left ventricular dysfunction on cardiovascular events and death. The Survival and Ventricular Enlargement is a randomized, double-blind, placebo-controlled multicenter trial, which evaluated the efficacy of captopril vs. placebo in 2331 patients following acute MI with left ventricular dysfunction defined as an ejection fraction less than or equal to 40%. Patients were randomly assigned to captopril or placebo 3 to 16 days following MI and were followed for 2 to 5 years. Among the 2231, 496 were patients with a history of diabetes, of which 168 were treated with insulin. Patients with diabetes were significantly older; more likely to be women; have a history of prior MI or hypertension; be obese or manifest Killip class II or greater; and have higher systolic blood pressure, pulse pressure, and heart rate, as well lower ejection fraction. During follow-up 31.3% of patients with diabetes and 20.1% of nondiabetic died. Furthermore, 50% of patients with diabetes had at least 1 major cardiovascular event compared with 32.3% among the nondiabetic patients. In multivariate analysis that adjusted for all significant differences in baseline characteristics, patients with diabetes had a 39% higher mortality and 49% more cardiovascular events. Among the patients with diabetes, baseline insulin treatment was associated with a greater risk of death and cardiovascular events. They concluded that in patients who survived MI with left ventricular dysfunction, diabetes increased risk of death from all causes even when controlling for differences in other risk factors. Patients with diabetes treated with insulin have a particularly higher mortality risk. Patients with diabetes who survived MI with left ventricular dysfunction, in particular those receiving insulin, are at high risk of subsequent mortality and cardiovascular events and this requires intensive risk factor modification, as well as evaluation for novel therapies.
Diabetes Care 27:2784-2789, 2004 has an excellent article titles Diet, growth, and risk for type 1 diabetes in childhood by Austé Pundziute-Lyckå, PHD et al. from Sweden. The study examined the association between type 1 diabetes risk and various intake of energy, accounting for body size and previous intake of nutriments and foods, accounting for energy intake. They conducted an incident population-based case- referent study in Stockholm including 99 of 100 eligible 7- to 14-year old diabetic children and 180 of 200 age, sex-, and are-matched referent children identified through the Swedish population register. Average daily energy and nutrient intake 1 year before diabetes diagnosis/interview was estimated using the food frequency questionnaire with assessment of consumed food amounts. Mean SD scores of growth measurements taken during the last 4 tears before diagnosis were used. Odds ratios (ORs) were calculated by conditional logistic regression. Average intake of energy, carbohydrate, fat, and protein was significantly higher among the case subjects as well as mean weight-for –age SD score. Higher energy intake and weight-for-age were both associated with increased diabetes risk after adjustment for each other: OR (95% CI) for medium and high levels of energy intake were 1.33 and 5.23 respectively, and for weight-for –age were 3.20 and 3.09 respectively. High intake of carbohydrates, especially disaccharides and sucrose, increased diabetes risk. The researchers concluded that higher energy intake and larger body size were independently associated with increased diabetes risk. Of the different nutriments, higher intake of carbohydrates, particularly disaccharides and sucrose, increased risk. Lifestyle habits leading to higher energy intake and more rapid growth in childhood may contribute to increased childhood-onset type 1 diabetes by different mechanisms.
Our last abstract comes from Diabetes Care 27:2856-2862, 2004. Depressive symptoms, insulin resistance, and risk of diabetes in women at midlife is written by Susan A. Everson-Rose, PHD, MPH et al. The researchers examined depression and 3-year change in insulin resistence and risk of diabetes and whether associations were by race. They analyzed data from 2,662 Caucasian, African-American, Hispanic, Japanese-American, and Chinese-American women without a history of diabetes from the Study of Women’s Health Across the Nation. They estimated regression coefficients and odds ratios to determine whether depression predicated increases in homeostasis model assessment of insulin resistence (HOMA-IR) and greater risk of incident diabetes, respectively, over 3 years. Mean baseline HOMA-IR was 1.31 and increased 0.05 units per year for all women. A total of 97 incident cases of diabetes occurred. Depression was associated with absolute levels of HOMA-IR but was unrelated to changes in HOMA-IR; associations did not vary by race. The association between depression and HOMA-IR was eliminated after adjustment for central adiposity. Depression predicted a 1.66-fold greater risk of diabetes, which became nonsignificant after adjustment for central adiposity. They also observed a depression-by-race interaction in analysis limited to Caucasians and African Americans the only groups with enough diabetes cases to reliably test this interaction. Race-stratified models showed that depression predicted 2.56-fold greater risk of diabetes in African Americans only, after risk factor adjustment. They concluded that depression is associated with higher HOMA-IR values and incident diabetes in middle-aged women. These associations are mediated through central adiposity. However, African-American women with depression experience increased risk of diabetes independent of central adiposity and other risk factors.
BSP
