For the first times since I started this column eleven years ago, it’s going to be about me. I was diagnosed with Type 2 Diabetes two weeks ago. While people are happy to talk about their experiences with diabetes, I WASN’T comfortable with talking about diabetes. My wife is Type 2, as are several friends of ours. The “other Type” of diabetes was what caused the death of my Best Man a year after my wife and I got married. He was diagnosed with diabetes when he was a kid. It was called Juvenile Diabetes then. Today it’s Type 1. Since then, I haven’t WANTED to talk about diabetes at all. But…for my own education and maybe helping someone else, and not one to shut up for any known reason, I’m reopening my blog rather than starting a new one. I MAY take a pause and write about Breast Cancer or Alzheimer’s as medical headlines dictate; but this time I’m going to drag anyone along who wants to join my HIGHLY RELUCTANT journey toward better understanding of my life with Type 2 Diabetes. You’re Welcome to join me!
When I started this whole Type 2 Diabetes adventure, I simply assumed that I could never touch sucrose (table sugar and the stuff that makes donuts and frosted cupcakes TASTE so amazing) for the rest of my life.
In fact, I thought that until a couple of days ago, my wife (who is also diagnosed with Type 2 diabetes), said to me, “I had potato chips last night – why are my blood sugars sky high?” (Or something to that effect…I’m 66 now! I can hardly remember the names of my three grandkids!)
I started wondering and after a recent Peanut Buster Parfait from Dairy Queen gave me a blood glucose the next morning of 158 (usually my morning glucose levels are around 170) and my most recent morning glucose was 179 with no obvious sugar bump in sight, I thought I’d better do some research.
Jody Stanislaw, ND, in her article, “The Many Reasons for High and Low Blood Sugars (and why we need a LOT of compassion for ourselves!)” at TCOYD (Taking Control of Your Diabetes) notes, “First of all, all carbs are not created equal. If you eat 30 grams of carbs from pineapple, it will raise blood sugar much, much faster than 30 grams of carbs from a low glycemic food, like black beans.”
OK. Cool. But what the heck does that MEAN?
Let’s dig: a cup of pineapple chunks has 16 grams of sugar; a cup of black beans has .28 grams of sugar…yet BOTH can have a detrimental effect on your blood glucose levels!
WTH???? Blood glucose and the foods you eat is an intensely complicated equation and MULIPLE things can have an impact on your glucose numbers!
BUT IN THE LONG RUN IT ALL COMES DOWN TO GLUCOSE! Glucose itself is an incredibly simple molecule (with the fancy pants chemical “formula” for glucose is C6H12O6 (C stands for carbon, H stands for Hydrogen, and O stands for Oxygen – hooked up in a particular way, it makes glucose. The number tell me how many of that atom there are in the sugar or fat or protien.)
While glucose isn’t a molecule you see the formula for, most people have seen H2O and know it’s the symbol for WATER! There are some more complicated sugars as well like sucrose (table sugar): C12H22O11 and fructose (fruit sugar) C6H12O6 – the SAME NUMBERS OF Carbon, Hydrogen, and Oxygen as GLUCOSE!!!! But it’s HOW the atoms are hooked up that make fructose twice as sweet as blood sugar.
Carbs are ALL made up of the same basic piece repeated twice to literally 10,000 times!
What’s black bean protein look like? It’s extremely complicated, which explains why it takes SO LONG to break it down in your blood. Usually you get saponins. Saponins, anthocyanins, flavonols, phenolic acids, and proanthocyanidins. I’ll show you just one: saponin?
Here’s its simplified H2O-kind of formula: C58H94O27. It takes a MUCH longer time for your stomach to break all those atoms up into glucose! The sugar in the fruit (in the form of fructose as well as sucrose) is EASILY available when it hits the blood because it arrives there as ALMOST glucose. The “sugar” in black beans comes from your stomach acid hitting the big carbohydrates and breaking them up into glucose – which takes awhile (it’s called digestion!) until they’ve been cut up until they show up on your blood sugar testing MUCH later.
With beans, you have to deal with FIBER, ‘cause they’re high in fiber.
Again, the formula for FIBER is even longer than the one for saponin but it’s not because its complicated, it’s because it’s a simple molecule that HOOKED TOGETHER INTO LONG STRINGS (you’d call them fibers!)
Cellulose is an organic compound with the formula (C6H10O5 yep, it’s basically a glucose molecule…that can be repeated INFINITELY) that is hooked up to form chains somewhere between of a few hundred to chains that hold over ten thousand glucose molecules. That’s why FIBER makes you feel full and then takes forever to break down into glucose when it can FINALLY be used by your body.
Then there are FATS which usually have slight variations on this molecule: C54H108O6
So, if I look at the bits and pieces of what I eat – if I’m eating sugars, they break down fast and slam into my blood sometimes in MINUTES. Fats take FOREVER to break down ‘cause they’re so big – they won’t slam my blood sugar for hours or maybe even days! If I eat fiber, I feel fuller and the sugars only leak off, having a minimal effect on my blood sugars.
So – my DQ Peanut Buster Parfait is mostly made up of the simpler sugars and takes little time to break down; where potato chips are mostly starch and oils – which take a MUCH LONGER TIME to break down into the glucose that shows up on my glucometer.
My DQ treat shows up early; the bag of chips show up late.
Source: https://tcoyd.org/2022/04/the-many-reasons-for-high-and-low-blood-sugars-and-why-we-need-a-lot-of-compassion-for-ourselves/?utm_source=google_cpc&utm_medium=ad_grant&utm_campaign=awareness&gad=1&gclid=CjwKCAjw8ZKmBhArEiwAspcJ7q9caZmUUmWbdd7o9TODGXdOL8BzGR-M090tEZmjYq5P1-pbxf3s6BoCcG0QAvD_BwE ,
Image: https://www.hcd.com/wp-content/uploads/2021/01/living-well-with-diabetes.jpg
A NEWLY DIAGNOSED T2 DIABETIC, breast cancer husband's observations mixed up with an Alzheimer's son's musings
Sunday, July 30, 2023
Sunday, July 16, 2023
DIABETES RESEARCH RIGHT NOW! #7: Will There EVER Be A Real CURE For Type 2?
From the first moment I discovered I had been diagnosed with DIABETES, I joined a HUGE “club” that has been rapidly expanding since it stopped being a death sentence in the early 20th Century. Currently, there are about HALF A BILLION PEOPLE who have Type 2 Diabetes. For the past 3500 years – dating back to Ancient Egypt – people have suffered from diabetes. Well, I’m one of them now… Not one to shut up for any known reason, I added a section to this blog…
Every month, I’ll be highlighting Diabetes research that is going on RIGHT NOW! Harvested from different websites, journals and podcasts, I’ll translate them into understandable English and share them with you. Today: STARTING with a 2014 article, “Diabetes – Will it Ever be cured?”; I check up on the various therapies mentioned…
1) “researchers have found evidence that beta cells do not burn out and die as previously thought, but instead revert to more primitive cells or ones with altered function, leading some scientists to believe that if they can prevent this dedifferentiation or somehow push dedifferentiated cells to turn back into beta cells, they could prevent or cure type 2 diabetes.”
June 26, 2023: “A proof-of-concept study demonstrates that ductal cells derived from the human pancreas can be influenced by pharmacological stimulation to regenerate beta-like cells that functionally release insulin, providing new hope for people living with diabetes.” (https://medicalxpress.com/news/2023-06-reactivation-beta-like-cells-pancreas-insulin.html) CLEARLY, the research is still in its infancy, BUT, what was simply hopeful thoughts is now moving into hopeful research. While this is also primarily a response to Type 1 diabetes, future investigation may yield a cure for Type 2.
2) “At Columbia University in New York, a team led by Domenico Accili, MD, professor of medicine, has made several discoveries about FOXO1, a protein that controls when genes are switched on or off.
“In research published in the March 11, 2012, Nature Genetics, the team found that deactivating FOXO1 in progenitor cells in the small intestines of newborn mice resulted in the cells becoming insulin-producing cells. In follow-up research published in the June 30, 2014, Nature Communications, Accili’s team conducted similar experiments in human intestinal cells derived from stem cells. Within seven days of FOXO1 deactivation, the cells began to produce insulin in response to glucose.”
While current research is looking specifically at cancer, “Therefore gaining a deeper understanding of FOXO family regulation, in addition to providing targeting opportunities for the development of novel therapies, may reveal robust FOXO-related pharmacological/prognostic biomarkers to enhance the clinical management and survival prospects of patients.” DE-activating this molecule appears to result in the reduction in cancer growth: “Several studies suggest that genetic variation in the FoxO1 gene is a predisposing factor for type 2 diabetes (T2D) or DKD [Diabetic Kidney Disease] in humans, revealing that FoxO1 may be involved in the initiation and development of DKD in patients with T2D, which provides new insight into the etiology of DKD.” (https://www.frontiersin.org/articles/10.3389/fphar.2021.630617/full)
3) “Another team, led by Rohit N. Kulkarni, MD, PhD, principal investigator at Joslin and associate professor of medicine at Harvard Medical School, published a paper in the January 2014, Diabetes in which they identified immune cells in mice that had minimal effects on destroying beta cells in type 1 and instead actually promoted their growth.
“King says that this research could be just as important for type 2 as type 1. “Even if we can’t get rid of the insulin resistance in type 2, we might be able to generate enough beta cells to overcome the insulin resistance and get rid of diabetes,” he says.”
Today, again in reference to Type 1 diabetes: “However, molecular spikes have significantly improved single cell mRNA accounting, adoption of the molecular spike method and further improvements may help address the above issues. As such, genuine SC-β cells will eventually become available as donor cells for establishing curative therapies for people suffering from T1DM in the not too distant future.”
In English? An RNA spike-in is a short bit of RNA of known sequence and quantity used to calibrate measurements in RNA how well this piece has attached to a section of DNA. Then, a specific amount of this RNA spike-in is mixed with an experiment sample. The amount of the RNA that shows up in the DNA is used to tweak the RNA so that the PANCREAS cells will stimulate the growth of NEW cells to replace the ones destroyed and thereby bring insulin production back to normal. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173812/, https://en.wikipedia.org/wiki/RNA_spike-in
4) “The gist is that we are trying to indirectly tweak T cells, which will help protect the beta cells from destruction,” Tisch says. “Different cytokines can affect different T cells, so the catch is figuring out which ones are the most effective.”
“Although widespread genetic therapies that could cure diabetes are still years away, such innovative research offers hope for the 382 million people across the globe with diabetes.”
This avenue appears to have started bearing fruit, admittedly in dealing with Type 1 – which is, I remind you, ultimately deadly – which Type 2 is NOT in the short run (If you’re interested, ask about my best man…) “Rather than developing new forms of insulin or insulin delivery, targeting immune modulation, or repurposing existing T2D drugs…The beneficial effects of [these new] drugs appear to effect beta-cells [which make insulin]. Beta cells are found in the pancreas…In type 1 diabetes, the body's immune system mistakenly destroys numbers, function, or survival [of the beta cells].” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10253164/
Again, the trickle down from Type 1 research is certain to reach those of us with Type 2!
Link: https://endocrinenews.endocrine.org/sept-2014-diabetes-will-it-ever-be-cured/,
https://www.healthline.com/health-news/diabetes-the-top-discoveries-and-developments-of-2022
Image: https://asploro.com/wp-content/uploads/2019/12/Diabetes-Research_Open-Access.jpg
Every month, I’ll be highlighting Diabetes research that is going on RIGHT NOW! Harvested from different websites, journals and podcasts, I’ll translate them into understandable English and share them with you. Today: STARTING with a 2014 article, “Diabetes – Will it Ever be cured?”; I check up on the various therapies mentioned…
1) “researchers have found evidence that beta cells do not burn out and die as previously thought, but instead revert to more primitive cells or ones with altered function, leading some scientists to believe that if they can prevent this dedifferentiation or somehow push dedifferentiated cells to turn back into beta cells, they could prevent or cure type 2 diabetes.”
June 26, 2023: “A proof-of-concept study demonstrates that ductal cells derived from the human pancreas can be influenced by pharmacological stimulation to regenerate beta-like cells that functionally release insulin, providing new hope for people living with diabetes.” (https://medicalxpress.com/news/2023-06-reactivation-beta-like-cells-pancreas-insulin.html) CLEARLY, the research is still in its infancy, BUT, what was simply hopeful thoughts is now moving into hopeful research. While this is also primarily a response to Type 1 diabetes, future investigation may yield a cure for Type 2.
2) “At Columbia University in New York, a team led by Domenico Accili, MD, professor of medicine, has made several discoveries about FOXO1, a protein that controls when genes are switched on or off.
“In research published in the March 11, 2012, Nature Genetics, the team found that deactivating FOXO1 in progenitor cells in the small intestines of newborn mice resulted in the cells becoming insulin-producing cells. In follow-up research published in the June 30, 2014, Nature Communications, Accili’s team conducted similar experiments in human intestinal cells derived from stem cells. Within seven days of FOXO1 deactivation, the cells began to produce insulin in response to glucose.”
While current research is looking specifically at cancer, “Therefore gaining a deeper understanding of FOXO family regulation, in addition to providing targeting opportunities for the development of novel therapies, may reveal robust FOXO-related pharmacological/prognostic biomarkers to enhance the clinical management and survival prospects of patients.” DE-activating this molecule appears to result in the reduction in cancer growth: “Several studies suggest that genetic variation in the FoxO1 gene is a predisposing factor for type 2 diabetes (T2D) or DKD [Diabetic Kidney Disease] in humans, revealing that FoxO1 may be involved in the initiation and development of DKD in patients with T2D, which provides new insight into the etiology of DKD.” (https://www.frontiersin.org/articles/10.3389/fphar.2021.630617/full)
3) “Another team, led by Rohit N. Kulkarni, MD, PhD, principal investigator at Joslin and associate professor of medicine at Harvard Medical School, published a paper in the January 2014, Diabetes in which they identified immune cells in mice that had minimal effects on destroying beta cells in type 1 and instead actually promoted their growth.
“King says that this research could be just as important for type 2 as type 1. “Even if we can’t get rid of the insulin resistance in type 2, we might be able to generate enough beta cells to overcome the insulin resistance and get rid of diabetes,” he says.”
Today, again in reference to Type 1 diabetes: “However, molecular spikes have significantly improved single cell mRNA accounting, adoption of the molecular spike method and further improvements may help address the above issues. As such, genuine SC-β cells will eventually become available as donor cells for establishing curative therapies for people suffering from T1DM in the not too distant future.”
In English? An RNA spike-in is a short bit of RNA of known sequence and quantity used to calibrate measurements in RNA how well this piece has attached to a section of DNA. Then, a specific amount of this RNA spike-in is mixed with an experiment sample. The amount of the RNA that shows up in the DNA is used to tweak the RNA so that the PANCREAS cells will stimulate the growth of NEW cells to replace the ones destroyed and thereby bring insulin production back to normal. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173812/, https://en.wikipedia.org/wiki/RNA_spike-in
4) “The gist is that we are trying to indirectly tweak T cells, which will help protect the beta cells from destruction,” Tisch says. “Different cytokines can affect different T cells, so the catch is figuring out which ones are the most effective.”
“Although widespread genetic therapies that could cure diabetes are still years away, such innovative research offers hope for the 382 million people across the globe with diabetes.”
This avenue appears to have started bearing fruit, admittedly in dealing with Type 1 – which is, I remind you, ultimately deadly – which Type 2 is NOT in the short run (If you’re interested, ask about my best man…) “Rather than developing new forms of insulin or insulin delivery, targeting immune modulation, or repurposing existing T2D drugs…The beneficial effects of [these new] drugs appear to effect beta-cells [which make insulin]. Beta cells are found in the pancreas…In type 1 diabetes, the body's immune system mistakenly destroys numbers, function, or survival [of the beta cells].” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10253164/
Again, the trickle down from Type 1 research is certain to reach those of us with Type 2!
Link: https://endocrinenews.endocrine.org/sept-2014-diabetes-will-it-ever-be-cured/,
https://www.healthline.com/health-news/diabetes-the-top-discoveries-and-developments-of-2022
Image: https://asploro.com/wp-content/uploads/2019/12/Diabetes-Research_Open-Access.jpg
Sunday, July 2, 2023
GUY’S GOTTA TALK ABOUT…DIABETES #11: Where’d Type 2 Diabetes Come From?
For the first times since I started this column eleven years ago, it’s going to be about me. I was diagnosed with Type 2 Diabetes two weeks ago. While people are happy to talk about their experiences with diabetes, I WASN’T comfortable with talking about diabetes. My wife is Type 2, as are several friends of ours. The “other Type” of diabetes was what caused the death of my Best Man a year after my wife and I got married. He was diagnosed with diabetes when he was a kid. It was called Juvenile Diabetes then. Today it’s Type 1. Since then, I haven’t WANTED to talk about diabetes at all. But…for my own education and maybe helping someone else, and not one to shut up for any known reason, I’m reopening my blog rather than starting a new one. I MAY take a pause and write about Breast Cancer or Alzheimer’s as medical headlines dictate; but this time I’m going to drag anyone along who wants to join my HIGHLY RELUCTANT journey toward better understanding of my life with Type 2 Diabetes. You’re Welcome to join me!
So, I grew up totally ignorant of diabetes.
My family didn’t talk about it. My high school health class didn’t talk about it. My college biology classes didn’t talk about it.
So, when first my wife, then myself were diagnosed with Type 2 diabetes, we were startled…
When did this whole Type 2 diabetes thing start?
Funny you should ask: “A disease characterised by the ‘too great emptying of urine’ finds its place in antiquity through Egyptian manuscripts dating back to 1500 B.C.1 Indian physicians called it madhumeha (‘honey urine’) because it attracted ants. The ancient Indian physician, Sushruta, and the surgeon Charaka (400–500 A.D.) were able to identify the two types, later to be named Type I and Type II diabetes…”
Besides my pee smelling sweet and attracting ants, what ELSE gave it away? (I’m staying away from Type 1 because that’s serious business and the man I asked to be best in my wedding, died a bit over a year later from complications due to his Type 1 (then called juvenile onset) diabetes, leaving a wife with a young child as well as a second child on-the-way…and while no death is pretty, his was pretty hideous…)
Type 2 has an interesting history that is pretty much hand-in-hand with the discovery and treatment of Type 1. “The ancient Roman doctor Galen mentioned diabetes but noted that he had only ever seen two people with it, which suggests that it was relatively rare in those days. By the fifth century C.E., people in India and China had worked out that there was a difference between type 1 and type 2 diabetes.
“They noted that type 2 diabetes was more common in heavy, wealthy people than in other people. At that time, this might have implied that these individuals ate more than other people and were less active. Nowadays, [with] the ready supply of processed food [that] has weakened the association between wealth and eating more…obesity, diet, and a lack of exercise are still risk factors for type 2 diabetes.”
So, it was identified – who figured out what the real problem was? Where did “insulin resistance” come into the picture? Discovered by the British scientist Harold Percival Himsworth, he found that with insulin resistance, a person’s body cells lose their sensitivity to insulin and are not able to take in glucose. ALL cells need to use insulin to work and divide to make new cells. Because of that, the pancreas increases its output of insulin to “force” the cells to take enough glucose to run well. As this continues to happen, it puts stress on the pancreas, damaging it. But, more than seven decades after that discovery, our knowledge of insulin action at whole-body, tissue, cellular, and intracellular levels remain far from complete. We DO know that Type 2 diabetic insulin resistance is involved with polycystic ovary syndrome, a very common hormone problem for women of childbearing age. Causing loss of ovulation, high levels of androgens, and small cysts on the ovaries; missed or irregular menstrual periods, excess hair growth, acne, infertility, and weight gain. ALL people with Type 2 diabetes can experience sleep disturbances, and pathological brain ageing.
So, the Type 2 diabetes is serious, but we CAN deal with it – typically using metformin (a first line response), as well as the dreaded E’s: Eat right and Exercise…
While I love writing, my primary purpose for all three conditions I’ve written on: breast cancer, Alzheimer’s, and Type 2 diabetes – is to teach myself what the HECK is going on around me, and now with Type 2, what’s going on inside of ME.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749019/#b2-squmj1303-368-370; https://www.medicalnewstoday.com/articles/317484#early-science ; https://onlinelibrary.wiley.com/doi/full/10.1111/j.1464-5491.2011.03488.x
Image: https://www.hcd.com/wp-content/uploads/2021/01/living-well-with-diabetes.jpg
So, I grew up totally ignorant of diabetes.
My family didn’t talk about it. My high school health class didn’t talk about it. My college biology classes didn’t talk about it.
So, when first my wife, then myself were diagnosed with Type 2 diabetes, we were startled…
When did this whole Type 2 diabetes thing start?
Funny you should ask: “A disease characterised by the ‘too great emptying of urine’ finds its place in antiquity through Egyptian manuscripts dating back to 1500 B.C.1 Indian physicians called it madhumeha (‘honey urine’) because it attracted ants. The ancient Indian physician, Sushruta, and the surgeon Charaka (400–500 A.D.) were able to identify the two types, later to be named Type I and Type II diabetes…”
Besides my pee smelling sweet and attracting ants, what ELSE gave it away? (I’m staying away from Type 1 because that’s serious business and the man I asked to be best in my wedding, died a bit over a year later from complications due to his Type 1 (then called juvenile onset) diabetes, leaving a wife with a young child as well as a second child on-the-way…and while no death is pretty, his was pretty hideous…)
Type 2 has an interesting history that is pretty much hand-in-hand with the discovery and treatment of Type 1. “The ancient Roman doctor Galen mentioned diabetes but noted that he had only ever seen two people with it, which suggests that it was relatively rare in those days. By the fifth century C.E., people in India and China had worked out that there was a difference between type 1 and type 2 diabetes.
“They noted that type 2 diabetes was more common in heavy, wealthy people than in other people. At that time, this might have implied that these individuals ate more than other people and were less active. Nowadays, [with] the ready supply of processed food [that] has weakened the association between wealth and eating more…obesity, diet, and a lack of exercise are still risk factors for type 2 diabetes.”
So, it was identified – who figured out what the real problem was? Where did “insulin resistance” come into the picture? Discovered by the British scientist Harold Percival Himsworth, he found that with insulin resistance, a person’s body cells lose their sensitivity to insulin and are not able to take in glucose. ALL cells need to use insulin to work and divide to make new cells. Because of that, the pancreas increases its output of insulin to “force” the cells to take enough glucose to run well. As this continues to happen, it puts stress on the pancreas, damaging it. But, more than seven decades after that discovery, our knowledge of insulin action at whole-body, tissue, cellular, and intracellular levels remain far from complete. We DO know that Type 2 diabetic insulin resistance is involved with polycystic ovary syndrome, a very common hormone problem for women of childbearing age. Causing loss of ovulation, high levels of androgens, and small cysts on the ovaries; missed or irregular menstrual periods, excess hair growth, acne, infertility, and weight gain. ALL people with Type 2 diabetes can experience sleep disturbances, and pathological brain ageing.
So, the Type 2 diabetes is serious, but we CAN deal with it – typically using metformin (a first line response), as well as the dreaded E’s: Eat right and Exercise…
While I love writing, my primary purpose for all three conditions I’ve written on: breast cancer, Alzheimer’s, and Type 2 diabetes – is to teach myself what the HECK is going on around me, and now with Type 2, what’s going on inside of ME.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749019/#b2-squmj1303-368-370; https://www.medicalnewstoday.com/articles/317484#early-science ; https://onlinelibrary.wiley.com/doi/full/10.1111/j.1464-5491.2011.03488.x
Image: https://www.hcd.com/wp-content/uploads/2021/01/living-well-with-diabetes.jpg
Sunday, June 18, 2023
DIABETES RESEARCH RIGHT NOW! #6: Trial Runs Of ARTIFICIAL PANCREAS Successful for Type 2 Diabetes Patients!!!!!
From the first moment I discovered I had been diagnosed with DIABETES, I joined a HUGE “club” that has been rapidly expanding since it stopped being a death sentence in the early 20th Century. Currently, there are about HALF A BILLION PEOPLE who have Type 2 Diabetes. For the past 3500 years – dating back to Ancient Egypt – people have suffered from diabetes. Well, I’m one of them now… Not one to shut up for any known reason, I added a section to this blog…
Every month, I’ll be highlighting Diabetes research that is going on RIGHT NOW! Harvested from different websites, journals and podcasts, I’ll translate them into understandable English and share them with you. Today: Well, JUST LOOK AT THE HEADLINE ABOVE!!!!
At the University of Cambridge (England), researchers have successfully developed on of the first devices that might be used to treat Type 2 Diabetes: “The device -- powered by an algorithm developed at the University of Cambridge -- doubled the amount of time patients were in the target range for glucose compared to standard treatment and halved the time spent experiencing high glucose levels.”
Now, does that mean we can all run out, throw away our Ozempic pens [to the joy and relief of all the really…um…weighty people for whom drugs like Ozempic are…um…a great HELP in their continuing…uh…“battle” against…er…Inexplicable High Mass Syndrome (IHMS, aka, being fat…)…].
At the University of Cambridge (England), researchers have successfully developed on of the first devices that might be used to treat Type 2 Diabetes: “The device -- powered by an algorithm developed at the University of Cambridge -- doubled the amount of time patients were in the target range for glucose compared to standard treatment and halved the time spent experiencing high glucose levels.”
Now, does that mean we can all run out, throw away our Ozempic pens [to the joy and relief of all the really…um…weighty people for whom drugs like Ozempic are…um…a great HELP in their continuing…uh…“battle” against…er…Inexplicable High Mass Syndrome (IHMS, aka, being fat…)…].
HOLD YOUR HORSES, BABA LOUIE! If you read the first sentence of the Science Daily article SLOWLY instead of skipping all words and leaving ONLY what I read as: “This [MIRACLE] device…doubled the amount of time…you can ignore your diabetes and eat whatever you want!"
My mind THINKS it's reading ‘patients were in the target range for glucose…and halved the time spent experiencing high glucose levels’. But then, my mind tends to be out to lunch in matters of what it can and can't direct my insulin-resistant body to do!
In case you’re new to this whole Type 2 diabetes thing, what is Type 2 diabetes? The English can explain it pretty well, “Type 2 diabetes causes levels of glucose -- blood sugar -- to become too high. Ordinarily, blood sugar levels are controlled by the release of insulin, but in type 2 diabetes insulin production is disrupted. Over time, this can cause serious problems including eye, kidney and nerve damage and heart disease.”
What that means is that…well, the outcome of our Type 2 diabetes is NOT trivial (which is sometimes what I allow myself to think – the whole, “Oh, I live in the 21st Century and I’m SURE that there’ll be a miracle cure pretty soon, so I don’t have to go all weird and stop eating doughnuts and drinking REGULAR soda, and I can eat like I’m 13 again. You just need to take on the ‘correct’ perspective…”
Anyway, the new device works something like this: For those of us with Type 2, it’s a fully closed loop system. The people for whom the device was originally developed – the ones with Type 1 have to “text” their artificial pancreas to let it know that they’ll be eating a meal. The AP (Artificial Pancreas) adjustment the amount of insulin it releases. For someone with Type 1, the AP adjusts automatically – just like your normal pancreas does.
The researchers recruited 26 patients. One group would use the AP eight weeks, then switch to doing multiple daily insulin injections. The other group would do multiple daily insulin injections for eight weeks, then switch to the AP.
The researchers monitored several things.
First: how much time did the patients spend with their glucose levels within a target range. They found that patients using the artificial pancreas spent two-thirds of their time on target. The other group only spent one third of their time on target.
Second: how much time spent did they have glucose levels 180? Average glucose levels fell from 170 to 106 about 70% of the time! The people using the insulin injections spent the same amount of time over 170!
Also, after using insulin injections, the average HbA1c levels were 8.7. Using the artificial pancreas they were 7.3!
By now you know that for those of us with Type diabetes, the higher the A1c, the greater the risk of developing diabetes-related complications. “Over time, high A1C levels may lead to impaired fasting glucose, high blood pressure, obesity, and an increased risk of cardiovascular diseases.”
When all was said and done, the researchers found that “…participants were happy to have their glucose levels controlled automatically by the system, and nine out reported spending less time managing their diabetes overall. Users highlighted the elimination of the need for injections or finger prick testing, and increased confidence in managing blood glucose as key benefits.” As is usual, not EVERYONE was happy with the AP. Some reported “…increased anxiety about the risk of hypoglycemia, which the researchers say may reflect increased awareness and monitoring of glucose levels, and practical annoyances with wearing of devices.”
All-in-all, I think if I could get this TEST DEVICE right now, I’d volunteer to be first in line!
Link: (ScienceDaily) https://scontent-dfw5-1.xx.fbcdn.net/v/t39.30808-6/354064720_646111904223281_7263858063343004950_n.jpg?stp=dst-jpg_p526x296&_nc_cat=101&ccb=1-7&_nc_sid=0debeb&_nc_ohc=ZihRXv-v-1sAX-1jkdq&_nc_ht=scontent-dfw5-1.xx&oh=00_AfBqk3DsoM2Y_v7tOlwbVKCMsaYoQooSsd_VrctAhwqmEA&oe=64933E1E; (The ACTUAL Article from the University of Cambridge (England): https://www.cam.ac.uk/research/news/artificial-pancreas-successfully-trialled-for-use-by-type-2-diabetes-patients
Image: https://asploro.com/wp-content/uploads/2019/12/Diabetes-Research_Open-Access.jpg
In case you’re new to this whole Type 2 diabetes thing, what is Type 2 diabetes? The English can explain it pretty well, “Type 2 diabetes causes levels of glucose -- blood sugar -- to become too high. Ordinarily, blood sugar levels are controlled by the release of insulin, but in type 2 diabetes insulin production is disrupted. Over time, this can cause serious problems including eye, kidney and nerve damage and heart disease.”
What that means is that…well, the outcome of our Type 2 diabetes is NOT trivial (which is sometimes what I allow myself to think – the whole, “Oh, I live in the 21st Century and I’m SURE that there’ll be a miracle cure pretty soon, so I don’t have to go all weird and stop eating doughnuts and drinking REGULAR soda, and I can eat like I’m 13 again. You just need to take on the ‘correct’ perspective…”
Anyway, the new device works something like this: For those of us with Type 2, it’s a fully closed loop system. The people for whom the device was originally developed – the ones with Type 1 have to “text” their artificial pancreas to let it know that they’ll be eating a meal. The AP (Artificial Pancreas) adjustment the amount of insulin it releases. For someone with Type 1, the AP adjusts automatically – just like your normal pancreas does.
The researchers recruited 26 patients. One group would use the AP eight weeks, then switch to doing multiple daily insulin injections. The other group would do multiple daily insulin injections for eight weeks, then switch to the AP.
The researchers monitored several things.
First: how much time did the patients spend with their glucose levels within a target range. They found that patients using the artificial pancreas spent two-thirds of their time on target. The other group only spent one third of their time on target.
Second: how much time spent did they have glucose levels 180? Average glucose levels fell from 170 to 106 about 70% of the time! The people using the insulin injections spent the same amount of time over 170!
Also, after using insulin injections, the average HbA1c levels were 8.7. Using the artificial pancreas they were 7.3!
By now you know that for those of us with Type diabetes, the higher the A1c, the greater the risk of developing diabetes-related complications. “Over time, high A1C levels may lead to impaired fasting glucose, high blood pressure, obesity, and an increased risk of cardiovascular diseases.”
When all was said and done, the researchers found that “…participants were happy to have their glucose levels controlled automatically by the system, and nine out reported spending less time managing their diabetes overall. Users highlighted the elimination of the need for injections or finger prick testing, and increased confidence in managing blood glucose as key benefits.” As is usual, not EVERYONE was happy with the AP. Some reported “…increased anxiety about the risk of hypoglycemia, which the researchers say may reflect increased awareness and monitoring of glucose levels, and practical annoyances with wearing of devices.”
All-in-all, I think if I could get this TEST DEVICE right now, I’d volunteer to be first in line!
Link: (ScienceDaily) https://scontent-dfw5-1.xx.fbcdn.net/v/t39.30808-6/354064720_646111904223281_7263858063343004950_n.jpg?stp=dst-jpg_p526x296&_nc_cat=101&ccb=1-7&_nc_sid=0debeb&_nc_ohc=ZihRXv-v-1sAX-1jkdq&_nc_ht=scontent-dfw5-1.xx&oh=00_AfBqk3DsoM2Y_v7tOlwbVKCMsaYoQooSsd_VrctAhwqmEA&oe=64933E1E; (The ACTUAL Article from the University of Cambridge (England): https://www.cam.ac.uk/research/news/artificial-pancreas-successfully-trialled-for-use-by-type-2-diabetes-patients
Image: https://asploro.com/wp-content/uploads/2019/12/Diabetes-Research_Open-Access.jpg
Sunday, June 4, 2023
GUY’S GOTTA TALK ABOUT…DIABETES #10: Can I REALLY Get Rid of Diabetes By Losing Weight and EATING Right?
For the first times since I started this column eleven years ago, it’s going to be about me. I was diagnosed with Type 2 Diabetes two weeks ago. While people are happy to talk about their experiences with diabetes, I WASN’T comfortable with talking about diabetes. My wife is Type 2, as are several friends of ours. The “other Type” of diabetes was what caused the death of my Best Man a year after my wife and I got married. He was diagnosed with diabetes when he was a kid. It was called Juvenile Diabetes then. Today it’s Type 1. Since then, I haven’t WANTED to talk about diabetes at all. But…for my own education and maybe helping someone else, and not one to shut up for any known reason, I’m reopening my blog rather than starting a new one. I MAY take a pause and write about Breast Cancer or Alzheimer’s as medical headlines dictate; but this time I’m going to drag anyone along who wants to join my HIGHLY RELUCTANT journey toward better understanding of my life with Type 2 Diabetes. You’re Welcome to join me!
Simple Answer to the title above is: Nope.
“…there's no cure for type 2 diabetes.”
“However, studies show it's possible for some people to reverse it. Through diet changes and weight loss, you may be able to reach and hold normal blood sugar levels without medication. This DOES NOT MEAN YOU’RE CURED. Type 2 diabetes is an ongoing disease. Even if you're in remission, which means you aren't taking medication and your blood sugar levels stay in a healthy range, there's always a chance that symptoms will return.”
So…how come there’s research going on in the UK (which has medical practices and health care easily comparable to what we have here in the US) with the intent of people reaching remission and not having to use diabetic meds – and that kind of research IS NOT HAPPENING HERE?
The only article I could find published in an American journal had this to say: “There is a plethora of treatment options available for patients with T2DM [aka Type 2 Diabetes], yet less than half achieve treatment goals. Current conventional clinical practices have proven largely unsuccessful in attaining adequate glycemic control and maintaining HbA1c under the recommended standard of 7.0%. Importantly, this is not due to a failure of therapeutic innovation. Over the last 20 years, several novel and promising anti-diabetes medications and technologies have been developed with consistent improvements in glycemic efficacy…metabolic surgical methods…intensive lifestyle modification plans.”
“Despite this, uncontrolled T2DM continues to have [gotten worse]…Given that evidence demonstrates that early glycemic control is paramount to avoiding microvascular complications and disease progression, this standard of care is unacceptable.”
Sorry, folks – it’s not the standard of care; it’s not the availability of programs; it’s not that there ARE no programs.
The problem, folks – is US.
Witness the wild scramble to get hold of Ozempic (semaglutide); Victoza (liraglutide); Rybelsus (semaglutide); Trulicity (dulaglutide); and many, many others – but NOT to control Type 2 Diabetes – stamping their feet and threatening lawsuits in their doctor’s office because at a high enough dosage, these can all MAKE YOU LOSE WEIGHT without that nasty, sweaty “exercise” thing; or that horrible, restrictive “diet” thing; we go right to our usual mode of operation: demanding that the world and whatnot is what we INSIST it to be rather than what it IS.
Drugs used to treat Type 2 Diabetes are the fat American’s answer to popping a pill and eating whatever you want. THERE’S NO EFFORT REQUIRED! We’ve been looking for this Golden Nugget for forever. We want to eat and then take a pill (or a shot) and “watch the pounds melt away”. You all see the ads, they pop up alongside pretty much whatever type of social media you use.
The problem is that it’s an American problem. The British study is pretty clear on how you and I can send Type 2 Diabetes into remission – but the method is full of nasty words: “diet change”, “weight loss”, “low calorie”, “restricted diet”, “more physical activity”, “bariatric surgery” – I mean, these all involve me DOING SOMETHING that’s not stuffing my face with donuts, candy, bread, cereal, whole milk, cream cheese puffs, potato chips, super-hyper-monstrous Burgers and sixteen orders of fries with melted cheese and ranch dip…
“Several studies in England have looked at the effects of a very low-calorie diet on overweight people with diabetes. Two had people follow a mostly liquid diet of 625-850 calories a day for 2-5 months, followed by a less restricted diet designed to help them keep off the weight they lost. Both studies found that nearly half the people who took part reversed their diabetes and kept their blood glucose near the normal range for at least 6 months to a year.”
The saddest sentence in the two articles came from the American study: “Despite evolution in treatment options and improved understanding of pathophysiology, the treatment of type 2 diabetes remains unsatisfactory.” And folks, it’s not the METHODS that aren’t working – it’s US who aren’t working.
Americans have come to expect “instant answers” and have a “one shot cures it all!” attitude. The pandemic only served to reinforce this attitude. While 6,900,000 people died, the world has pretty much decided that with vaccines, COVID-19 is done and we can go back to normal life.
It’s my opinion that Type 2 Diabetes hasn’t reached that point yet, but most people who suffer from it are waiting patiently for the “one shot cures it all!” – and many have decided that the drugs used by patients who actually have been diagnosed with Type 2 HAVE to be used so those who love to overeat can CONTINUE to overeat with impunity – just take a shot a week and BAM! Back to the troughs!
Jaundiced POV? Nah, jaundice is a DIFFERENT disease.
Source: UK: https://www.webmd.com/diabetes/can-you-reverse-type-2-diabetes#:~:text=Although%20there's%20no%20cure%20for,diabetes%20is%20an%20ongoing%20disease. ; US: https://www.mdpi.com/2673-4540/4/1/11
Image: https://www.hcd.com/wp-content/uploads/2021/01/living-well-with-diabetes.jpg
Simple Answer to the title above is: Nope.
“…there's no cure for type 2 diabetes.”
“However, studies show it's possible for some people to reverse it. Through diet changes and weight loss, you may be able to reach and hold normal blood sugar levels without medication. This DOES NOT MEAN YOU’RE CURED. Type 2 diabetes is an ongoing disease. Even if you're in remission, which means you aren't taking medication and your blood sugar levels stay in a healthy range, there's always a chance that symptoms will return.”
So…how come there’s research going on in the UK (which has medical practices and health care easily comparable to what we have here in the US) with the intent of people reaching remission and not having to use diabetic meds – and that kind of research IS NOT HAPPENING HERE?
The only article I could find published in an American journal had this to say: “There is a plethora of treatment options available for patients with T2DM [aka Type 2 Diabetes], yet less than half achieve treatment goals. Current conventional clinical practices have proven largely unsuccessful in attaining adequate glycemic control and maintaining HbA1c under the recommended standard of 7.0%. Importantly, this is not due to a failure of therapeutic innovation. Over the last 20 years, several novel and promising anti-diabetes medications and technologies have been developed with consistent improvements in glycemic efficacy…metabolic surgical methods…intensive lifestyle modification plans.”
“Despite this, uncontrolled T2DM continues to have [gotten worse]…Given that evidence demonstrates that early glycemic control is paramount to avoiding microvascular complications and disease progression, this standard of care is unacceptable.”
Sorry, folks – it’s not the standard of care; it’s not the availability of programs; it’s not that there ARE no programs.
The problem, folks – is US.
Witness the wild scramble to get hold of Ozempic (semaglutide); Victoza (liraglutide); Rybelsus (semaglutide); Trulicity (dulaglutide); and many, many others – but NOT to control Type 2 Diabetes – stamping their feet and threatening lawsuits in their doctor’s office because at a high enough dosage, these can all MAKE YOU LOSE WEIGHT without that nasty, sweaty “exercise” thing; or that horrible, restrictive “diet” thing; we go right to our usual mode of operation: demanding that the world and whatnot is what we INSIST it to be rather than what it IS.
Drugs used to treat Type 2 Diabetes are the fat American’s answer to popping a pill and eating whatever you want. THERE’S NO EFFORT REQUIRED! We’ve been looking for this Golden Nugget for forever. We want to eat and then take a pill (or a shot) and “watch the pounds melt away”. You all see the ads, they pop up alongside pretty much whatever type of social media you use.
The problem is that it’s an American problem. The British study is pretty clear on how you and I can send Type 2 Diabetes into remission – but the method is full of nasty words: “diet change”, “weight loss”, “low calorie”, “restricted diet”, “more physical activity”, “bariatric surgery” – I mean, these all involve me DOING SOMETHING that’s not stuffing my face with donuts, candy, bread, cereal, whole milk, cream cheese puffs, potato chips, super-hyper-monstrous Burgers and sixteen orders of fries with melted cheese and ranch dip…
“Several studies in England have looked at the effects of a very low-calorie diet on overweight people with diabetes. Two had people follow a mostly liquid diet of 625-850 calories a day for 2-5 months, followed by a less restricted diet designed to help them keep off the weight they lost. Both studies found that nearly half the people who took part reversed their diabetes and kept their blood glucose near the normal range for at least 6 months to a year.”
The saddest sentence in the two articles came from the American study: “Despite evolution in treatment options and improved understanding of pathophysiology, the treatment of type 2 diabetes remains unsatisfactory.” And folks, it’s not the METHODS that aren’t working – it’s US who aren’t working.
Americans have come to expect “instant answers” and have a “one shot cures it all!” attitude. The pandemic only served to reinforce this attitude. While 6,900,000 people died, the world has pretty much decided that with vaccines, COVID-19 is done and we can go back to normal life.
It’s my opinion that Type 2 Diabetes hasn’t reached that point yet, but most people who suffer from it are waiting patiently for the “one shot cures it all!” – and many have decided that the drugs used by patients who actually have been diagnosed with Type 2 HAVE to be used so those who love to overeat can CONTINUE to overeat with impunity – just take a shot a week and BAM! Back to the troughs!
Jaundiced POV? Nah, jaundice is a DIFFERENT disease.
Source: UK: https://www.webmd.com/diabetes/can-you-reverse-type-2-diabetes#:~:text=Although%20there's%20no%20cure%20for,diabetes%20is%20an%20ongoing%20disease. ; US: https://www.mdpi.com/2673-4540/4/1/11
Image: https://www.hcd.com/wp-content/uploads/2021/01/living-well-with-diabetes.jpg
Sunday, May 21, 2023
DIABETES RESEARCH RIGHT NOW! #6: PART 1 Where We've Come From, Where We're Going
From the first moment I discovered I had been diagnosed with DIABETES, I joined a HUGE “club” that has been rapidly expanding since it stopped being a death sentence in the early 20th Century. Currently, there are about HALF A BILLION PEOPLE who have Type 2 Diabetes. For the past 3500 years – dating back to Ancient Egypt – people have suffered from diabetes. Well, I’m one of them now… Not one to shut up for any known reason, I added a section to this blog…
Every month, I’ll be highlighting Diabetes research that is going on RIGHT NOW! Harvested from different websites, journals and podcasts, I’ll translate them into understandable English and share them with you. Today: From the discovery of diabetes to the POSSIBILITY of a pancreas transplant...
So, I’m under treatment for my Type 2 diabetes. But I was wondering the other day: “What’s the GOAL of what I’m doing now – watching the diet, monitoring my blood glucose levels, taking Metformin…WHERE AM I GOING?”
As far as I have been able to tell from talking with my doctor and researching my condition for the past year, the “goal” seems to be “Live with Type 2 as good as you can so you won’t get all the complications you can get before you die an early death…”
Given I live in the first half of the 21st Century and we regularly talk about artificial intelligence, smart phones, missions to Mars, private space craft flying to an international space station…where heart-lung transplants (first done here in my home town, Minneapolis) and quintuple heart bypasses are *yawningly* routine…why is our solution for Type 2 diabetes just, “Well, ya got it, so learn to live with it. No pancreas transplant for YOU!!!!”
Hmmm…I’m not sure I’m OK with that any more…
In a 2011 interview for the Arizona Republic newspaper/website, Black American memoirist, poet, and civil rights activist, Maya Angelou said, “If you don't know where you've come from, you don't know where you're going.”
While this is clearly true for her life’s work, it’s also as true and useful an aphorism as it can be. In fact, I can see the straightforward application to my life with Type 2 diabetes.
Most of us know that diabetes is one of THE best known and understood diseases, having been diagnosed originally over 3000 years ago by an Egyptian physician named Hesy-Ra, who documented what we would call Type One diabetes from patients who had frequent urination and along with extreme weight loss. The name originated in 230 BC, by the Greek physician named, Apollonius of Memphis. And in 1675 Thomas Willis, an English physician, added the Greek word mellitus to the word diabetes. This was because those with diabetes had urine that smelled sweet (it also tasted sweet, but let’s not go THERE…)
Then, we reach the 20th Century “Frederick M. Allen was a physician in 1913, who believed that previous diabetic treatments had been ineffective because they attempted to substitute fats for carbohydrates which ended with the patient in a coma and dying! Only a starvation diet that limited the total caloric consumption was effective. Allen found that a liquids-only diet could eliminate glycosuria and acidosis. The diabetic could then begin to eat gradually increasing diets, until sugar again began to show up in the urine. This test would allow him to determine how many calories a patient could safely consume. This was LONG before the discovery of insulin. He also recognized that diabetes was not just a disease that caused elevated blood sugar levels but also problems with metabolism.”
In 1936, two doctors discovered insulin in 1921; the next year, a young boy with Type 1 was injected with it…and “the cure” had arrived. Insulin first came from animals – dogs initially; then cows, oxen, and others in 1936…and this was standard practice.
Until suddenly, in 1982, artificially produced, genetically engineered HUMAN-EQUIVALENT insulin made using yeast cells and E. coli (yeah, the one that can give you horrendous diarrhea…) was approved by the FDA and released for use in the world population of Type 1 diabetics. The treatment for diabetes changed dramatically.
And yet…no CURE. A treatment. Certainly stunning, and yet, what about US? Type 2 diabetics? Insulin RESISTANCE was introduced in 1936. The first line of defense has become Metformin. What is it? “…first described in scientific literature in 1922, it was introduced as a medication in France in 1957 and the United States in 1995. In 2020, it was the third most commonly prescribed medication in the United States”
In two weeks…more about metformin – and some concern a friend of mine pointed out…and the possibilities of an artificial, transplantable pancreas!
Link: https://type2diabetes.com/living/10-facts-history-diabetes, https://en.wikipedia.org/wiki/Insulin, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6205949/, https://en.wikipedia.org/wiki/Metformin Image: https://asploro.com/wp-content/uploads/2019/12/Diabetes-Research_Open-Access.jpg
Every month, I’ll be highlighting Diabetes research that is going on RIGHT NOW! Harvested from different websites, journals and podcasts, I’ll translate them into understandable English and share them with you. Today: From the discovery of diabetes to the POSSIBILITY of a pancreas transplant...
So, I’m under treatment for my Type 2 diabetes. But I was wondering the other day: “What’s the GOAL of what I’m doing now – watching the diet, monitoring my blood glucose levels, taking Metformin…WHERE AM I GOING?”
As far as I have been able to tell from talking with my doctor and researching my condition for the past year, the “goal” seems to be “Live with Type 2 as good as you can so you won’t get all the complications you can get before you die an early death…”
Given I live in the first half of the 21st Century and we regularly talk about artificial intelligence, smart phones, missions to Mars, private space craft flying to an international space station…where heart-lung transplants (first done here in my home town, Minneapolis) and quintuple heart bypasses are *yawningly* routine…why is our solution for Type 2 diabetes just, “Well, ya got it, so learn to live with it. No pancreas transplant for YOU!!!!”
Hmmm…I’m not sure I’m OK with that any more…
In a 2011 interview for the Arizona Republic newspaper/website, Black American memoirist, poet, and civil rights activist, Maya Angelou said, “If you don't know where you've come from, you don't know where you're going.”
While this is clearly true for her life’s work, it’s also as true and useful an aphorism as it can be. In fact, I can see the straightforward application to my life with Type 2 diabetes.
Most of us know that diabetes is one of THE best known and understood diseases, having been diagnosed originally over 3000 years ago by an Egyptian physician named Hesy-Ra, who documented what we would call Type One diabetes from patients who had frequent urination and along with extreme weight loss. The name originated in 230 BC, by the Greek physician named, Apollonius of Memphis. And in 1675 Thomas Willis, an English physician, added the Greek word mellitus to the word diabetes. This was because those with diabetes had urine that smelled sweet (it also tasted sweet, but let’s not go THERE…)
Then, we reach the 20th Century “Frederick M. Allen was a physician in 1913, who believed that previous diabetic treatments had been ineffective because they attempted to substitute fats for carbohydrates which ended with the patient in a coma and dying! Only a starvation diet that limited the total caloric consumption was effective. Allen found that a liquids-only diet could eliminate glycosuria and acidosis. The diabetic could then begin to eat gradually increasing diets, until sugar again began to show up in the urine. This test would allow him to determine how many calories a patient could safely consume. This was LONG before the discovery of insulin. He also recognized that diabetes was not just a disease that caused elevated blood sugar levels but also problems with metabolism.”
In 1936, two doctors discovered insulin in 1921; the next year, a young boy with Type 1 was injected with it…and “the cure” had arrived. Insulin first came from animals – dogs initially; then cows, oxen, and others in 1936…and this was standard practice.
Until suddenly, in 1982, artificially produced, genetically engineered HUMAN-EQUIVALENT insulin made using yeast cells and E. coli (yeah, the one that can give you horrendous diarrhea…) was approved by the FDA and released for use in the world population of Type 1 diabetics. The treatment for diabetes changed dramatically.
And yet…no CURE. A treatment. Certainly stunning, and yet, what about US? Type 2 diabetics? Insulin RESISTANCE was introduced in 1936. The first line of defense has become Metformin. What is it? “…first described in scientific literature in 1922, it was introduced as a medication in France in 1957 and the United States in 1995. In 2020, it was the third most commonly prescribed medication in the United States”
In two weeks…more about metformin – and some concern a friend of mine pointed out…and the possibilities of an artificial, transplantable pancreas!
Link: https://type2diabetes.com/living/10-facts-history-diabetes, https://en.wikipedia.org/wiki/Insulin, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6205949/, https://en.wikipedia.org/wiki/Metformin Image: https://asploro.com/wp-content/uploads/2019/12/Diabetes-Research_Open-Access.jpg
Sunday, May 7, 2023
GUY’S GOTTA TALK ABOUT…DIABETES #9: The “Dawn Phenomenon” and What Does That Mean???
For the first times since I started this column eleven years ago, it’s going to be about me. I was diagnosed with Type 2 Diabetes two weeks ago. While people are happy to talk about their experiences with diabetes, I WASN’T comfortable with talking about diabetes. My wife is Type 2, as are several friends of ours. The “other Type” of diabetes was what caused the death of my Best Man a year after my wife and I got married. He was diagnosed with diabetes when he was a kid. It was called Juvenile Diabetes then. Today it’s Type 1. Since then, I haven’t WANTED to talk about diabetes at all. But…for my own education and maybe helping someone else, and not one to shut up for any known reason, I’m reopening my blog rather than starting a new one. I MAY take a pause and write about Breast Cancer or Alzheimer’s as medical headlines dictate; but this time I’m going to drag anyone along who wants to join my HIGHLY RELUCTANT journey toward better understanding of my life with Type 2 Diabetes. You’re Welcome to join me!
I was diagnosed with Type 2 Diabetes six and a half months ago and have been monitoring, working on losing weight, eating right, and taking my Metformin…
According to the World Health Organization, “The expected values for normal fasting blood glucose concentration are between 70 mg/dL and 100 mg/dL. When fasting blood glucose is between 100 to 125 mg/dL, changes in lifestyle and monitoring glycemia are recommended.” The lowest reading I’ve EVER had since this start was on April 14 – and that wasn’t even QUITE normal, it was 138. So, my glucometer data was ALL in the red and I get constant, nasty notes from the thing telling me my “Blood Glucose Levels have been high the last three times!” Honestly? No matter WHAT I did lowered the levels after fasting.
So, I changed my USER settings to 110-182 mg/dL. I didn’t do it to make myself feel PHYSICALLY better: I’d have changed it to 3000-1,000,000 mg/dL, then! I just got tired of getting beat up by my device, and imagining the people who set these limits look like this: https://aanmc.org/wp-content/uploads/2020/06/Dr.Duzzi2017Headshot-scaled-e1594240915188-906x1024.jpg
I needed a realistic goal; a realistic reflection of my experience with room to grow. So, then, what is the Dawn Phenomenon?
“The dawn phenomenon or ‘dawn effect’ is when your blood sugar spikes in the early-morning hours, usually between 3-8am. The dawn phenomenon is very common among those with insulin resistance, and there are some strategies that may help you reduce your fasting blood sugar. What causes are still unclear, though we know that hormones play a large part. These hormones follow a daily cycle, and increase during our waking hours, starting in the early morning.”
So what do I DO about it? The first thing I saw was this: “Working up a sweat in the a.m. is a good idea for anyone experiencing the dawn phenomenon, too—it can help burn up that extra blood glucose.”
GREAT; but I already do that – I bike between 4 and 9 miles every-other-morning and it hasn’t had ANY effect on my blood sugars – they’re the same whether I exercise or not.
Tick. So, as I am writing this on 5/4/23; tonight I will take my blood sugar before bed and then wake up at 2:30am and take them. By the time you read this, you’ll know the result.
What else? No snacks before bed? Uhhhh…I have my phone alarm set at 7 pm; with the intent of not eating anything afterwards. While I sometimes hit that goal, I sometimes miss it, too. I need to both work harder at meeting the goal and also record what I did. The Mayo Clinic Online says I should: “Avoid carbohydrates at bedtime. Change your dose of diabetes medicine or insulin. Switch to a different diabetes medicine. Change the time when you take your medication or insulin from dinnertime to bedtime. Use an insulin pump to give you extra insulin during early-morning hours.”
I’m going to opt for the first one: Avoid carbs at bedtime.
So: no snacks before bed/no carbs before bed (work harder at this); record my blood sugars before bed and in the middle of the night; (continue to) exercise in the morning.
That’s about it! I’ll let you know how it went.
Source: https://www.virtahealth.com/blog/dawn-phenomenon, https://www.mayoclinic.org/diseases-conditions/diabetes/expert-answers/dawn-effect/faq-20057937, https://diabetes.org/diabetes/treatment-care/high-morning-blood-glucose
Image: https://www.hcd.com/wp-content/uploads/2021/01/living-well-with-diabetes.jpg
I was diagnosed with Type 2 Diabetes six and a half months ago and have been monitoring, working on losing weight, eating right, and taking my Metformin…
According to the World Health Organization, “The expected values for normal fasting blood glucose concentration are between 70 mg/dL and 100 mg/dL. When fasting blood glucose is between 100 to 125 mg/dL, changes in lifestyle and monitoring glycemia are recommended.” The lowest reading I’ve EVER had since this start was on April 14 – and that wasn’t even QUITE normal, it was 138. So, my glucometer data was ALL in the red and I get constant, nasty notes from the thing telling me my “Blood Glucose Levels have been high the last three times!” Honestly? No matter WHAT I did lowered the levels after fasting.
So, I changed my USER settings to 110-182 mg/dL. I didn’t do it to make myself feel PHYSICALLY better: I’d have changed it to 3000-1,000,000 mg/dL, then! I just got tired of getting beat up by my device, and imagining the people who set these limits look like this: https://aanmc.org/wp-content/uploads/2020/06/Dr.Duzzi2017Headshot-scaled-e1594240915188-906x1024.jpg
I needed a realistic goal; a realistic reflection of my experience with room to grow. So, then, what is the Dawn Phenomenon?
“The dawn phenomenon or ‘dawn effect’ is when your blood sugar spikes in the early-morning hours, usually between 3-8am. The dawn phenomenon is very common among those with insulin resistance, and there are some strategies that may help you reduce your fasting blood sugar. What causes are still unclear, though we know that hormones play a large part. These hormones follow a daily cycle, and increase during our waking hours, starting in the early morning.”
So what do I DO about it? The first thing I saw was this: “Working up a sweat in the a.m. is a good idea for anyone experiencing the dawn phenomenon, too—it can help burn up that extra blood glucose.”
GREAT; but I already do that – I bike between 4 and 9 miles every-other-morning and it hasn’t had ANY effect on my blood sugars – they’re the same whether I exercise or not.
Tick. So, as I am writing this on 5/4/23; tonight I will take my blood sugar before bed and then wake up at 2:30am and take them. By the time you read this, you’ll know the result.
What else? No snacks before bed? Uhhhh…I have my phone alarm set at 7 pm; with the intent of not eating anything afterwards. While I sometimes hit that goal, I sometimes miss it, too. I need to both work harder at meeting the goal and also record what I did. The Mayo Clinic Online says I should: “Avoid carbohydrates at bedtime. Change your dose of diabetes medicine or insulin. Switch to a different diabetes medicine. Change the time when you take your medication or insulin from dinnertime to bedtime. Use an insulin pump to give you extra insulin during early-morning hours.”
I’m going to opt for the first one: Avoid carbs at bedtime.
So: no snacks before bed/no carbs before bed (work harder at this); record my blood sugars before bed and in the middle of the night; (continue to) exercise in the morning.
That’s about it! I’ll let you know how it went.
Source: https://www.virtahealth.com/blog/dawn-phenomenon, https://www.mayoclinic.org/diseases-conditions/diabetes/expert-answers/dawn-effect/faq-20057937, https://diabetes.org/diabetes/treatment-care/high-morning-blood-glucose
Image: https://www.hcd.com/wp-content/uploads/2021/01/living-well-with-diabetes.jpg
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