Question: what is the “Turkey Disease”?

Dr. Weeks’ Comment:  I refer to the illness of diabetes to my patients as “the turkey disease”.  Why? Because of two reasons both of which render the diabetic a tragic, for lack of a better word….  “turkey”.

1) the carving,  which results from poorly managed diabetes, starts at the toes then climbs to the BKO  (“below knee operation”) leaving a knee as stump, then the AKO (“above knee operation”) where the knee is carved off,  then other diseased tissues are removed. Like a turkey. 

2) the fact that this disease is preventable –   that is the second reason.  Prevention, as always,  is the best medicine here.

 (so, eat organic food to avoid the fungicide which sets up diabetes  – see second post below)

 

Treating Diabetes Early, Intensively Is Best Strategy, New Study Suggests

ScienceDaily (June 28, 2012) ”” Intensive early treatment of type 2 diabetes slows down progression of the disease by preserving the body’s insulin-producing capacity, a UT Southwestern study has shown.

“We can potentially change the course of this prevalent disease, which would represent a breakthrough,” said Dr. Ildiko Lingvay, assistant professor of internal medicine and author of the study published online in Diabetes Care. “The intensive treatment regimen we propose is different from the stepwise approach recommended in standard guidelines.”

As one of the fastest-growing diseases in the U.S., diabetes afflicts an estimated 25.8 million children and adults, or 8.3 percent of the population, according to the American Diabetes Association. A study by Population Health Management projects the number of diabetes cases to nearly double by 2025.

The UT Southwestern study was selected for presentation at the recent American Diabetes Association’s Diabetes Care Symposium and will be published in the July print issue of ADA’s Diabetes Care.

While intensive treatment has been the standard at UT Southwestern for at least a decade, the industry norm has been to emphasize lifestyle changes first. The American College of Physicians, for example, suggests losing weight and dieting before drug treatment. The ADA recommends similar lifestyle changes, plus the use of metformin — the standard drug used to treat type 2 diabetes — for those newly diagnosed.

“We believe that the stepwise approach exposes patients to long periods of high blood sugar, which leads to complications,” Dr. Lingvay said. “Unless dietary changes are significant and sustained long-term, diabetes is a progressive disease in which the body’s ability to produce insulin declines.”

If a patient can maintain insulin production, she explained, the disease is easier to manage. The study showed intensive treatment with insulin, followed by one of two drug regimens, enabled diabetes patients to maintain steady insulin-producing beta-cell function for three and a half years after diagnosis.

“This finding was true, regardless of the method used to attain intensive control,” Dr. Lingvay said. “Intensive treatments led to excellent control of blood-sugar levels, they were well-tolerated, safe, and had good compliance.”

In the UT Southwestern clinical trial, participants were randomly divided into two groups. Both groups first had three months of treatment with insulin and the anti-diabetes drug metformin. After that, one group took three types of diabetes medications daily, while the other continued the insulin and metformin treatment. Out of 63 initial trial recruits, 58 completed the study and are still being tracked for six-year results.

Dr. Lingvay said the study did not show that any single regimen worked better than another; both intensive treatment regimens were just as effective.

“The point is that whatever you choose, make sure it’s intensive,” she said. “We have shown that this preserves beta-cell function, and that’s the key in changing the course of the disease.”

Other UT Southwestern researchers involved in the study were Dr. Lindsay Harrison, an endocrinology fellow; Beverley Adams-Huet, assistant professor in clinical sciences and internal medicine; and Dr. Philip Raskin, professor of internal medicine.

The research was supported by grants from the National Institutes of Health and Novo Nordisk Inc., a supplier of insulin. Novo Nordisk played no role in the study design, conduct, analysis, preparation, or final approval.

Journal Reference:
  1. L. B. Harrison, B. Adams-Huet, P. Raskin, I. Lingvay. Cell Function Preservation After 3.5 Years of Intensive Diabetes TherapyDiabetes Care, 2012; 35 (7): 1406 DOI:10.2337/dc11-2170

 

AND

 

Fungicide Used On Farm Crops Linked to Insulin Resistance

ScienceDaily (June 25, 2012) ”” A fungicide used on farm crops can induce insulin resistance, a new tissue-culture study finds, providing another piece of evidence linking environmental pollutants to diabetes. The results were presented June 23 at The Endocrine Society’s 94th Annual Meeting in Houston.

“For the first time, we’ve ascribed a molecular mechanism by which an environmental pollutant can induce insulin resistance, lending credence to the hypothesis that some synthetic chemicals might be contributors to the diabetes epidemic,” said investigator Robert Sargis, M.D., Ph.D., instructor in the endocrinology division at the University of Chicago.

The chemical, tolylfluanid, is used on farm crops in several countries outside of the United States to prevent fungal infestation, and sometimes is used in paint on ships to prevent organisms from sticking to their hulls. Animal studies have indicated that the chemical may adversely affect the thyroid gland, as well as other organs, and that it may increase the risk of cancer in humans.

Within the last decade, research attention has increasingly focused on the link between environmental contaminants and the rising rates of obesity and diabetes throughout many parts of the world. In the United States alone, nearly 26 million adults and children have some form of diabetes, according to the American Diabetes Association. A serious disease by itself, diabetes also increases the risk of other medical complications, including heart and blood-vessel diseases.

Normally, the pancreas secretes the hormone insulin, which acts to regulate blood-sugar levels. Among diabetic patients, insulin secretion either decreases or stops altogether, or cells become resistant to the hormone’s activity. These conditions then disrupt the process that transports sugar, or glucose, from the blood to the body’s other cells, which can lead to the dangerously high blood-sugar levels associated with diabetes.

In this project, Sargis and his co-investigators used mouse fat to examine the effects of tolylfluanid on insulin resistance at the cellular level. They found that exposure to tolylfluanid induced insulin resistance in fat cells, which play a critical role in regulating the body’s blood glucose and fat levels. When exposed to tolylfluanid in culture the ability of insulin to trigger action inside the fat cell, or adipocyte, was reduced, which is an early indication of diabetes.

“The fungicide and antifouling agent tolylfluanid may pose a threat to public health through the induction of adipocytic-insulin resistance, an early step in the pathogenesis of type 2 diabetes,” Sargis said. “Based on these studies, further efforts should be undertaken to clarify human exposure to tolylfluanid and the possible metabolic consequences of that exposure.”

At the same time, tolylfluanid-exposed cells stored more fat, or lipids, in a similar action to a steroid called corticosterone. Like this steroid, tolylfluanid bound receptors in fat cells, called glucocorticoid receptors, which help regulate blood-sugar levels, as well as many other important body processes.

“For the public, this raises the specter of environmental pollutants as potential contributors to the metabolic disease epidemic,” said Sargis, adding that, “hopefully, it will put further pressure on public policy makers to reassess the contribution of environmental pollution as a contributor to human disease in order to encourage the development of strategies for reversing those effects.”

The National Institute of Environmental Health Sciences and the University of Chicago Diabetes Research and Training Center funded this research.

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