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  • karaka
    ... From: Fred Flanders MD GENE VARIANT INCREASES RISK OF TYPE 2 DIABETES But Healthy Lifestyle Changes Reduce Genetic Risk
    Message 1 of 1 , Aug 1, 2006
      ------ Forwarded Message

      From: "Fred Flanders MD" <fredflandersmd@...>  
      But Healthy Lifestyle Changes Reduce Genetic Risk

      Researchers have confirmed that a gene variant confers susceptibility to
      type 2 diabetes in participants of the Diabetes Prevention Program
      (DPP), a large clinical trial in adults at increased risk for developing
      type 2 diabetes. The finding, published in the July 20, 2006, issue of
      the "New England Journal of Medicine", follows the discovery by deCode
      Genetics that a variant in a gene called TCF7L2 predisposes people to
      type 2 diabetes.
      "The DPP is an outstanding example of a robust clinical trial that
      continues to answer crucial questions about the etiology and prevention
      of type 2 diabetes, a complex disease that is steadily rising throughout
      the nation and the world," said National Institutes of Health (NIH)
      Director Elias A. Zerhouni, M.D. The NIH, which sponsored the DPP,
      continues to fund the follow-up study of DPP participants.
      The researchers were delighted to observe that even the participants at
      highest genetic risk benefited from healthy lifestyle changes as much or
      perhaps more than those who did not inherit the variant. "The lifestyle
      intervention reduced risk even in those who carried both copies of the
      risk variant," said lead author Jose Florez, M.D., Ph.D., of
      Massachusetts General Hospital (MGH) in Boston. "This finding emphasizes
      that people at risk of diabetes, whether they're overweight, have
      elevated blood glucose levels, or have this particular genetic variant,
      can benefit greatly by implementing a healthy lifestyle."
      Launched in 1995, the DPP ended in 2001, a year earlier than planned
      because the results were so clear. The researchers published their main
      findings in 2002 (http://www.nih.gov/news/pr/feb2002/hhs-06.htm). The
      3,234 people who took part in the study were adults with blood glucose
      readings that were higher than normal but not yet in the diabetic range.
      Most were significantly overweight. Nearly half were minorities, who are
      at disproportionately high risk for diabetes. Those who lost 5 to 7
      percent of weight by cutting calories in their diet and increasing
      physical activity (e.g., walking 5 days a week 30 minutes a day) reduced
      the onset of type 2 diabetes by 58 percent. Treatment with metformin
      lowered the chances of developing diabetes by 31 percent.
      The DPP participants randomly assigned to lifestyle changes received
      guidance from a dietitian and lifestyle coach during the study. Most
      adults at risk for diabetes don't have access to such support. "Finding
      better ways to predict who is at greatest risk for developing diabetes
      might focus interventions on those most likely to benefit," says Sanford
      Garfield, Ph.D., of the National Institute of Diabetes and Digestive and
      Kidney Diseases (NIDDK), which spearheaded the DPP.
      The newly identified gene variant, or allele, is located on chromosome
      10q25.3. It is a single nucleotide polymorphism (SNP), or single base
      pair change, in the region of a gene that codes for a transcription
      factor -- a protein that acts like a "master switch" regulating the
      expression of other genes. In their DNA analysis, the researchers found
      one copy of the risk variant in 40 percent of DPP participants, and two
      copies in 10 percent. "For the 10 percent of people who inherited two
      copies of the variant, the risk of developing diabetes is about 80
      percent higher than it is for non-carriers," explained Dr. Florez.
      The DPP Genetics subgroup conducted the study in a multi-institutional
      collaborative effort.* Its findings build on the deCode Genetics report,
      published online in "Nature Genetics" in January 2006, by:
      -- confirming the finding in an independent population that included the
      racial and ethnic diversity typical of the U.S. population with diabetes
      -- showing that the gene variant increases risk in those with
      pre-diabetes, and in a prospective study where patients are followed
      over time
      -- examining for the first time the relationship between the genetic
      risk factor and interventions that delay diabetes onset, and
      -- showing that the gene variant affects insulin production, not cells'
      response to insulin.
      The hallmarks of type 2 diabetes are insulin resistance - the inability
      of target tissues to respond to insulin - and a gradual failure of beta
      cells to produce enough insulin. "This variant of TCF7L2 is associated
      with decreased insulin production, but not with any increase in insulin
      resistance," said DPP study chair David M. Nathan, M.D., of MGH.
      "Our data, combined with previous longitudinal studies and genetic
      findings, show that type 2 diabetes can be triggered by decreased
      insulin production and not just by insulin resistance. However,
      researchers need to learn more about this gene before they can even
      obesity; and kidney, urologic and hematologic diseases. Spanning the
      full spectrum of medicine and afflicting people of all ages and ethnic
      groups, these diseases encompass some of the most common, severe, and
      disabling conditions affecting Americans.
      The National Institutes of Health (NIH) -- "The Nation's Medical
      Research Agency" -- includes 27 Institutes and Centers and is a
      component of the U.S. Department of Health and Human Services. It is the
      primary federal agency for conducting and supporting basic, clinical and
      translational medical research, and it investigates the causes,
      treatments, and cures for both common and rare diseases. For more
      information about NIH and its programs, visit www.nih.gov.

      * Named authors included Jose Florez, Nick Bayley, Paul de Bakker, David
      M. Nathan and David Altshuler from MGH, Kathleen Jablonski from George
      Washington University, Toni Pollin and Alan Shuldiner from the
      University of Maryland, and William Knowler from NIDDK on behalf of the
      Diabetes Prevention Program Research Group

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