So, one year ago today I was given my Diabetes Type II diagnosis. I don't know an exact date for when my Diabetes developed, but I know that it was sometime between April 2010 (had bloodwork done & my numbers were normal at that time) and January 2011 ( had bloodwork done & my numbers were not normal). And based on symptoms I can even narrow that down a little more. We took our grandkids to Disney World in late May 2010 and I had no symptoms but by Thanksgiving I was experiencing hypoglycemic lows. So I have it narrowed down to a five month span of time. I'm going to lean closer to the end of that 5 month span since my symptoms are probably a good indicator. So we could say Fall 2010.
So much has changed in this past year with regards to my health and diet. I now know a lot of numbers regarding glucose, cholesterol, blood pressure and the likes that I had no clue about before my diagnosis. I was already on blood pressure medicine, but I just took the pill every day - no real knowledge or concern what the numbers were or meant. I was also on meds for my triglycerides. And again, I was just taking the pill - let the pill take care of the number. But once I was told I had Diabetes I realized that any and all of the health issues I was taking meds for would all become more important simply because Diabetes tends to complicate most health issues.
I also now know how, when and why to test my glucose. Who would have thought that pricking my finger daily would become such a non-event? But after the first few weeks it pretty much became a non- event. I do it almost without thought now. In fact, my 7 year old grand-daughter does the finger prick for me when she is here. For some reason she loves helping me with my Diabetes - be it fthe finger prick or reminding me that I can't eat sugar (not that I do anymore, but she will ask for a snack and tell me she would like a Kit Kat Candy Bar end then say "But you can't have it cause it has sugar, right?").
And, when first diagnosed, my BG and A1C were both so high that I was immediately put on Metformin and Insulin injections. And while the injections never became a non-event, it did get easier before it got better. Initially I had a herder time injecting myself so I had my husband do my injections, but God love him, I know he cared and I know he meant well, but I think he became too complacent after a few weeks and I started feeling the injections more than I thought I should. I knew that I needed to tough-up and do this myself. It wasn't all that bad and I actually got pretty good at it. But fortunately I was also making major changes to my diet and exercise and was able to get my blood glucose numbers into control well enough that I came off the insulin completely.
With continued diet modification (I can't say continued exercise since that has more or less fallen to the way-side - but honestly, who wants to stand in their den and do exercises all alone day after day - it is just so uninspiring and un-motivating to me.), but anyway, with continued diet I have managed to keep my BG controlled well enough that I eventually came off the Metformin also. Coming off Metformin was primarily to address major hair loss I was experiencing. I was shedding worse than a sheep dog in the dead of summer in South Alabama. I could walk from my bedroom to my kitchen and drop no less than 10 hairs on the way - and that is a short stroll in my tiny house. And, having now been off Metformin for a few months my hair loss has subsided. If ever my BG becomes too hard to control without meds I will address the hair loss issue at that time. But until then, I will stay the course and hope my diet keeps my glucose in good control for a long long time.
So, that brings me to my One Year Diaversary - and I now consider my Diabetes to be a non-event. It is a fact of life and a pert of who I am, but all in all it is currently just the impetus behind my diet choices. I will never eat sugar as I once did and I will forever choose diet drinks over regular drinks (something I wanted no part of prior to my diagnosis) and I will be selective and limiting in regard to carb foods.
My next goal is to reach my 5 year Diaversary without having to get back on any Diabetes meds. Here's to the next five years being non-events! (clink clink)
I don't expect to have to update this blog for five more years, so, until then, Goodnight Moon. :D
Showing posts with label In the News. Show all posts
Showing posts with label In the News. Show all posts
Tuesday, January 17, 2012
Tuesday, August 23, 2011
#Diabetes - Researchers Identify New Target for Treatment of Type 2 Diabetes and Prediabetes
Released: 8/22/2011 12:45 PM EDT
Source: Joslin Diabetes Center
Newswise — BOSTON — Aug. 22, 2011 — Researchers at the Joslin Diabetes Center have shown that an enzyme found in the mitochondria of cells is decreased in the skeletal muscle of those with type 2 diabetes, a finding that could lead to the development of drugs to boost the activity of this enzyme in an effort to fight the disease.
A paper in published online today in the Proceedings of the National Academy of Sciences, showed that the enzyme, Sirt3, is decreased in the skeletal muscle of humans and animals with diabetes by at least half, compared to those without diabetes and that this may contribute to development of insulin resistance, one of the earliest manifestations of the disease. Sirt3 is found in the mitochondria, the power producers of cells that convert energy into usable forms.
“Ours is perhaps the first study to understand what is going wrong in the mitochondria of those with diabetes,” said senior author C. Ronald Kahn, M.D., Head of the Joslin Section on Integrative Physiology and Metabolism and the Mary K. Iacocca Professor of Medicine at Harvard Medical School. “Many studies have shown that the mitochondria don’t work well in those with diabetes. This points to a cause of why they don’t work well.”
Dr. Kahn said the study sought to look at how decreased Sirt3 levels might affect the metabolism of cells, particularly how it could affect insulin action in cells. “We know that one of the hallmarks of early diabetes is insulin resistance in muscle, but we didn’t know what caused it,” he said.
He said the study showed that when Sirt3 levels are low, as they are in the case of diabetes, the mitochondria of the cells are not as efficient in energy metabolism as they should be.
When the mitochondria become inefficient, they generate what are known as reactive oxygen species (ROS), chemically reactive molecules containing oxygen, which create insulin resistance in the muscles, he said.
“This is the first time this has been shown,” Dr. Kahn said.
The goal for the future will be to find ways to restore levels of Sirt3 or increase the activity of the existing Sirt3, perhaps with a drug, in a bid to improve insulin resistance in the muscle and improve muscle metabolism, he said.
“It is a new target,” he said.
Dr. Kahn noted that this study is one of the first demonstrations of a single defect that could affect mitochondrial metabolism and insulin signaling in the muscle.
“In further studies we will try to understand what proteins Sirt3 acts on,” he said.
He noted that one of the earliest hallmarks of diabetes is insulin resistance in the skeletal muscle. As a result, a drug to boost Sirt3 levels could be useful in the treatment of prediabetes or in those newly diagnosed with the disease, he said.
“Agents which increase Sirt3 activity could, therefore, potentially reverse at least some of the adverse effects of type 2 diabetes,” the paper concludes.
Co-authors included Enxuan Jing, lead author, as well as Brice Emanuelli, Jeremie Boucher and Kevin Lee, all of Joslin; Matthew D. Hirschey and Eric M. Verdin, both of Gladstone Institute of Virology and Immunology and the University of California, San Francisco; and David Lombard, formerly of the Department of Genetics at Harvard Medical School and currently at the Department of Pathology and Institute of Gerontology at the University of Michigan.
Dr. Verdin noted that by “uncovering the multi-faceted role of SIRT3, we are laying important groundwork to better combat this widespread disease at the cellular level.”
The study was supported by research grants to Kahn and Verdin as well as a grant from the Ellison Foundation and the Mary K. Iacocca Professorship. The study also received support from the Joslin DERC cores laboratories.
Source: Joslin Diabetes Center
Newswise — BOSTON — Aug. 22, 2011 — Researchers at the Joslin Diabetes Center have shown that an enzyme found in the mitochondria of cells is decreased in the skeletal muscle of those with type 2 diabetes, a finding that could lead to the development of drugs to boost the activity of this enzyme in an effort to fight the disease.
A paper in published online today in the Proceedings of the National Academy of Sciences, showed that the enzyme, Sirt3, is decreased in the skeletal muscle of humans and animals with diabetes by at least half, compared to those without diabetes and that this may contribute to development of insulin resistance, one of the earliest manifestations of the disease. Sirt3 is found in the mitochondria, the power producers of cells that convert energy into usable forms.
“Ours is perhaps the first study to understand what is going wrong in the mitochondria of those with diabetes,” said senior author C. Ronald Kahn, M.D., Head of the Joslin Section on Integrative Physiology and Metabolism and the Mary K. Iacocca Professor of Medicine at Harvard Medical School. “Many studies have shown that the mitochondria don’t work well in those with diabetes. This points to a cause of why they don’t work well.”
Dr. Kahn said the study sought to look at how decreased Sirt3 levels might affect the metabolism of cells, particularly how it could affect insulin action in cells. “We know that one of the hallmarks of early diabetes is insulin resistance in muscle, but we didn’t know what caused it,” he said.
He said the study showed that when Sirt3 levels are low, as they are in the case of diabetes, the mitochondria of the cells are not as efficient in energy metabolism as they should be.
When the mitochondria become inefficient, they generate what are known as reactive oxygen species (ROS), chemically reactive molecules containing oxygen, which create insulin resistance in the muscles, he said.
“This is the first time this has been shown,” Dr. Kahn said.
The goal for the future will be to find ways to restore levels of Sirt3 or increase the activity of the existing Sirt3, perhaps with a drug, in a bid to improve insulin resistance in the muscle and improve muscle metabolism, he said.
“It is a new target,” he said.
Dr. Kahn noted that this study is one of the first demonstrations of a single defect that could affect mitochondrial metabolism and insulin signaling in the muscle.
“In further studies we will try to understand what proteins Sirt3 acts on,” he said.
He noted that one of the earliest hallmarks of diabetes is insulin resistance in the skeletal muscle. As a result, a drug to boost Sirt3 levels could be useful in the treatment of prediabetes or in those newly diagnosed with the disease, he said.
“Agents which increase Sirt3 activity could, therefore, potentially reverse at least some of the adverse effects of type 2 diabetes,” the paper concludes.
Co-authors included Enxuan Jing, lead author, as well as Brice Emanuelli, Jeremie Boucher and Kevin Lee, all of Joslin; Matthew D. Hirschey and Eric M. Verdin, both of Gladstone Institute of Virology and Immunology and the University of California, San Francisco; and David Lombard, formerly of the Department of Genetics at Harvard Medical School and currently at the Department of Pathology and Institute of Gerontology at the University of Michigan.
Dr. Verdin noted that by “uncovering the multi-faceted role of SIRT3, we are laying important groundwork to better combat this widespread disease at the cellular level.”
The study was supported by research grants to Kahn and Verdin as well as a grant from the Ellison Foundation and the Mary K. Iacocca Professorship. The study also received support from the Joslin DERC cores laboratories.
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