FYI: The 36th Annual Meeting of the Association for the Study of Diabetes will be held in Jerusalem, Israel, Sept.17 to 21, 2000. You can visit the site for information at http:/www.kenes.com/easd. This information comes to us from Yoav Kaaarari, the webmaster of the site. Thanks for the information.
We get questions monthly about the efficacy of taking dietary supplements with other medications and the drug-drug interactions. The Jan. 27th issue of JAMA has an article called "Diet Supplement Data on the Internet" by Charles Marwick which will help all of you who are looking for reliable information. The Office of Dietary Supplements (ODS) at the National Institutes Of Health (NIH) has started a database of bibliographic information on the Internet at http://dietary-supplements.info.nih.gov/ called the international Bibliographic Information on Dietary Supplements( IBIDS).
Currently the data base contains 300,000 citations from published scientific literature dating from 1986. It includes abstracts when available but not full reports. Bernadette M. Marriott, Ph.D., the director of the office hopes it will be useful to the scientific community and to the public. She said that pulling together the information was a huge task as it comes from a broad range of disciplines: botany, chemistry, pharmaceuticals, medicine, and agriculture. There are currently over 1000 key words to identify scientific information on dietary supplements. This site is a result of the 1994 Dietary Supplement Health and Education Act which directed NIH to provide support for research on supplements.
Although the citations in IBIDS are selected from peer-reviewed journals whenever possible, not all of them have been peer-reviewed. This is because some journals do not review each article anymore. Marriott concluded that users should exercise skepticism in evaluating citations and recommended looking at the methods of the study. "Ask yourself a few questions. How may subjects were in the study? How good is it? Is it relevant?" There may sufficient information in the abstracts, but Marriott suggests reading the original article to make your determinations about its validity.
January 8th Tulsa World newspaper included a Knight Rider article linking blood sugar to the miscarriage rate. Studies show that high level of blood sugar in the blood can cause cells of developing embryos to kill themselves. This is thought to be a reason that diabetic mothers have more miscarriages or babies with birth defects. The research done at Washington University in St. Louis studies diabetic mice. The researchers isolated very young embryos from diabetic mother mice and compared them with embryos of normal mice. Cells in the embryos from diabetic mice showed more signs of "apaptosis" or cellular suicide, when compared with the embryo cells from normal mother mice. When the researchers treated the diabetic mice with insulin, the mouse embryos were normal. The researchers concluded that the same cell suicide problems might occur in women with diabetes. If too many cells die in the very young embryos, certain organs might not be able to perform properly later on. That would result in miscarriage or a birth defect.
The Dec. 8, 1998 JAMA had a review of research done by the University of Toronto by Thomas M. Wolever et al, titled ’No Relationship Between Carbohydrate Intake and Effect of Acarbose on HbA1c or Gastrointestinal Symptoms in type 2 Diabetic Subjects Consuming 30-60% of Energy from Carbohydrates.’ The objective of the research was to determine the relationship between carbohydrate intake and the effect on HbA1c in subjects with type 2 diabetes treated with acarbose alone, acarbose plus sulfonylurea, acarbose plus metformin, or acarbose plus insulin. The research was a double blind randomized placebo-controlled study in which subjects with diabetes in four treatment groups (77 on diet alone, 83 treated with metformin, 103 treated with sulfonylurea and 91 treated with insulin) were randomized to treatment with placebo or acarbose for 12 months. Before randomization, and 3, 6, 9, and 12 months after randomization, fasting blood was obtained for HbA1c, and 3-day diet records were collected.
Conclusions indicated that in subjects with type 2 diabetes consuming 30-60% of energy from carbohydrates, the effect of acarbose on HbA1c, and gastrointestinal symptoms was not related to carbohydrate intake. Because most people consume at least 30% of energy from carbohydrate, the researchers concluded that no specific diet is needed for acarbose to be effective in improving blood glucose control on the treatment of type 2 diabetes.
Are you concerned about switching from beef-pork insulin to Humalin? Enough people are that JAMA had an article in the Jan.13, 1999 issue titles "Switch to Human Insulin Worries Some Diabetics" by Mike Mitka. The biggest fear among users of animal based insulin making the change, he states, is hypoglycemia unawareness. There are some people who fear they may develop hypoglycemia without the neurogenic warning symptoms they are used to so that they can take carbohydrates before it gets worse. Although hypoglycemia unawareness is real, it’s not because of an inherent difference in the effect of the insulin. People may experience a difference in the time course of the two products. Human insulin may act sooner and its duration may be shorter, so one has to monitor oneself more frequently.
John Holcombe, MD, a senior clinical physician at Lilly says that current research shows that switching to human-based insulin does not cause hypoglycemia unawareness. There is a lot of research to prove he is correct using double blind studies, both published in the Lancet and Diabetes Medicine. He agreed that the key is to get the dosing, timing, and self-monitoring correct to make the change-over successful.
Lilly ended production of beef-pork insulin because fewer than 5% (about 100,000) of insulin users take it and because the company couldn’t economically maintain its 25 different formulations for such a small and declining percentage of the population. Human insulin is now the world standard and offers benefits over animal-based insulin, such as fewer allergic reactions and avoidance of tissue changes at the site of injection. The ADA endorsed the switch over. Richard Kahn, Ph.D.. the ADA’s chief scientific and medical officer said "We’re a bit nervous, but biologically there should be no reason why you can’t switch- over. Now there are patients who claim they can’t switch. We don’t know why that’s so. but they should be working with their [physicians]to adjust dosage and other aspects". Eli Lilly has "Tips for Easing the Transfer to Human Insulin" which you can get from them or your health care team.
Shemer, A et al in the International Journal of Dermatology, Feb., 98 published an article titled ‘Diabetic Dermopathy and Internal Complications in Diabetes Mellitus.’ Knowing that diabetic dermopathy is the most common marker of diabetes, the researchers looked at the relationship of diabetic dermopathy to internal complications such as nephropathy, retinopathy, and neuropathy. One hundred and seventy-three patients with diabetes, of whom 125 (72%) had type 1 diabetes and 48 (28%) had type 2 diabetes were studied. Diabetic dermopathy was present in 69 (40%) of the patients, significantly more significant in patients 50 years of age or older. The mean diabetic duration was significantly higher in patients with diabetic dermopathy than in those without. The association of the condition with retinopathy, nephropathy, and neuropathy were statistically significant, and the increased frequency of diabetic dermopathy correlated with an increased number of these three complications. The researchers concluded that some of the factors that affect the development of internal complications in diabetes may play a role in the development of diabetic dermopathy and that this condition may serve as a clinical sign of an increased likelihood of these internal complications of diabetes.
Katherine Samaras, MBBS, FRACP et al in Diabetes Care, Vol. 21, No 12, 1999 writes about ‘Genetic Versus Environment, The Relationship Between Dietary Fat and Total Central Abdominal Fat’. The influence of diet on body fat has not been qualified independently of genetic influences, although both are thought to contribute to regulation of body fat stores. This study examined the relationship between recent diet and total body and abdominal fat in middle-aged female twins independent of genetic and important environmental factors, and the evidence of interaction between diet and genetic predisposition.
Measurement of 436 healthy female twins included dietary intake by food questionnaire, BMI. total body and central abdominal fat by duel-energy X-ray absorptiometry, and environmental covariants (smoking, hormone replacement, and physical activity) by standardized questionnaire.
Results indicated that intake of dietary fat (total and subtype) and carbohydrates was not related to BMI or to total or central fat. A minor inverse relationship between carbohydrate intake and total adiposity was confirmed. In paired analysis, the twin with the higher sugar intake of total sugars has significantly lower body and central abdominal adiposity. There was no evidence of a gene-environment interaction between intake of fat or carbohydrates contributing to greater body fat mass in subjects genetically predisposed to obesity. The researcher concluded that the role of dietary factors in determining total body and central abdominal fat appears to have been overestimated in past Cross-sectional studies.
Volume 22, Number 1, 1999 of Diabetes Care has an article by Amer G. Rassam, MD et al titled ‘Optimal Administration of Lispro Insulin in Hyperglycemic type 1 Diabetes.’ The reason for the study is to form recommendations for the optimal injection time of lispro insulin in patients who are hyperglycemic. The researchers hypothesized that in contrast to normoglycemic patients with diabetes, injection of lispro insulin 15-30 minutes before a meal would improve postprandial glucose excursion in hyperglycemic diabetic. The research team examined 48 randomized overnight studies. Twelve healthy adult type 1 diabetic patients received lispro insulin mixed with human ultralente at minutes (-30,-15,and +15) relative to the ingestion of an ADA breakfast of 8.6kcal/kg. Pre-breakfast hyperglycemia was established before the study by a continuous overnight infusion of intravenous insulin, which was stopped 30 minutes before the lispro insulin injection. Glucose and insulin levels were measured every 30 minutes for 5 hours after breakfast.
Results demonstrated that postprandial glucose excursion was reduced when lispro insulin was administered 15-30 minutes before the meal compared with lispro insulin injected at the meal. Although injecting lispro insulin at 30 minutes before the meal resulted in a significant reduction in postprandial glycemia, it was accompanied by loss of glucose control at 4 hours postmeal in two subjects. The researchers concluded that in hyperglycemic patients optimization of lispro insulin requires an injection at least 15 minutes before the meal.
Next month look for an interesting article just published titled "Sildenafil for the treatment of erectile dysfunction in men with diabetes."
