Tuesday, February 16, 2016

Protective Gene for Type 1

"A Finnish study has now revealed two genetic mutations which seem to
lower the risk of contracting a diabetic retinal or kidney disease."

Based on these results, "it seems that the SLC19A3 gene has a role in the development of diabetic nephropathy and diabetic retinopathy. The results also help explain why some patients with type 1 diabetes are more likely to develop complications than others, says Iiro Toppila, the researcher responsible for analysing the data. However, further research is needed into the biological effects of point mutations."

In the secret medalist group on Facebook, one medalist made the following statement:
"I was told by Joslin that I have the cell that either slows or stops
the complications of diabetes. I am 60 yrs with type 1 and am 62 yrs
old."

The Joslin Medalist Study has examined 1000 people with 50 or
more years of Type 1 diabetes. The purpose of the study is to find
what makes the medalists different from so many other type 1
individuals who have had diabetes related complications. The study
began in 2005, and is ongoing. I participated in the study in 2009. In
2011, I attended a medalist meeting at the Joslin Medical Center. Dr
King, head of the project, announced that a large group of the
participants in the study have some kind of "inner protection" that
has prevented them from having any serious complications with their
eyes, kidneys, and nervous systems. He also said that the inner
protection does not protect our hearts, and that we should do our best
to have good heart health. Many medalists have had heart by-passes. I
have been type 1 for 70 years, and except for some minor nerve
damage, I do not have any of these complications. My heart is also in
good shape. Perhaps the protective gene, or cell, is present in my body,
and in the bodies of so many other healthy long term type 1 diabetics.
That gene is certainly present in the bodies of so many younger type 1
diabetics, too.

Here is the link for the complete article:

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