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
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
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
