Sunday, October 6, 2024

GUY’S GOTTA TALK ABOUT…TYPE 2 DIABETES #25: Know What LEAD Stands For? [Neither Did I: Life Expectancy Estimator for Older Adults with Diabetes]

For the first time since I started this blog 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!


Did you know that there are medical standards of care that doctors can refer to when they’re working with seniors with Type 2 diabetes?

Neither did I.

Also, while the document was JUST revised in December of 2023, there’s an entire section that applies to seniors. One of the early sections had an interesting statement, and I’ll go through the part that applies to me and wife a bit later.

I was startled to find this: “The recommendations and text of Section 5 were adjusted to place focus on guiding the behavior of health care professionals rather than people with diabetes, thus aligning with the purpose of the Standards of Care as guidance for health care professionals.” (13. Older Adults: Standards of Care in Diabetes—2024)

One of the reasons for greater involvement and expected reliance on a person’s health care professional is something I’m SURE all of you are familiar with (if not with the fancy-pants name), “polypharmacy”. Never heard of it ‘til I read this document: “noun: polypharmacy; the simultaneous use of multiple drugs to treat a single ailment or condition; the simultaneous use of multiple drugs by a single patient, for one or more conditions.” I see it as “make sure you put the right pills in the right box so you can take them at the right time!”

I can see that – even though when I was trying to help my mother self-manage the numerous pills she had to take, the freakin’ condition didn’t have a NAME!) Of COURSE I need the advice of my doctor (who isn’t actually a DOCTOR per se, but a Physicians Assistant) to know when to take what I need to take and HOW to take it! Now the American Diabetes Association has made an official recommendation.

Another thing I’ll be talking to my PA about is this: “Notably, the Life Expectancy Estimator for Older Adults with Diabetes (LEAD) tool was developed and validated among older adults with diabetes, and a high-risk score was strongly associated with having a life expectancy of less-than five years.”

The heck is THIS????

Here’s what I found out: “A tool based on data from the electronic health record (EHR) may help clinicians estimate life expectancy in older adults with diabetes, a recent study found. The tool uses gender, body mass index, serum creatinine level, dementia, metastatic cancer, peripheral vascular disease, albuminuria, home oxygen use, wheelchair use, current smoking, and the interaction between age and heart failure to generate a risk score.”


They noted, “The authors noted that their tool…was not validated in patients younger than age 65 years and was less accurate over longer periods (among other limitations.) They also cautioned that the tool's results should be considered in a broader context along with other factors that influence individualized care, such as patient preferences.”

So…why would I get this test if it offers such limited amount of information? (The “conspiracy theorist in me would say, “So insurance companies can deny MORE seniors health care coverage…”) But, I’m CERTAIN that’s not what it would be used for! It’s a tool to…what?

I suppose looking at ALL of those things, would give a doctor or other caregiver different things to both watch for and begin to work on. For example: body mass index – if I knew my BMI was too high, I could certainly start to work to lose weight. Nothing STUPID, but certainly change the fact that I eat a package of OREO Cookie DoubleStufs before bed once a week! I could stop smoking (if I did, but I didn’t, so let’s just go back to eating Oreos); I could get screened for Alzheimer’s (which I do twice a year); I could make sure I exercise regularly to keep my heart strong (I ride about 12-15 miles a week during the summer; and stationary bike 2-5 hours a week in the winter in addition to walking a couple of miles every other day.)

I could have my PA give me the LEAD: Life Expectancy Estimator for Older Adults with Diabetes (LEAD)…which I will when I go in for my shots in a week or so…I’ll report then!

Source: https://diabetesjournals.org/care/article/47/Supplement_1/S244/153944/13-Older-Adults-Standards-of-Care-in-Diabetes-2024; https://diabetesjournals.org/care/article/47/Supplement_1/S5/153943/Summary-of-Revisions-Standards-of-Care-in-Diabetes; 13. Older Adults: Standards of Care in Diabetes—2024 | Diabetes Care | American Diabetes Association (diabetesjournals.org) Image: https://www.hcd.com/wp-content/uploads/2021/01/living-well-with-diabetes.jpg

Sunday, September 22, 2024

DIABETES RESEARCH RIGHT NOW! #21: FIRST EVER CURE FOR TYPE 2 DIABETES!!!! (SELF-Harvested Stem Cell) Therapy

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: Repairing the Pancreas!


While the headline is from a report from China published this past May, the DREAM of restarting a pancreas damaged enough to initiate Type 2 diabetes has been around at least since 2011.

Today, there is not only hope that this might happen, but AT LEAST ONE person whose Type 2 diabetes was reversed using his own treated stem cells to regrow pancreas cells in large enough numbers to reinitiate his body’s production of the correct amount of insulin.

In the September 2011 issue of Genome Medicine, the author wrote: “Stem cells hold great promise for pancreatic beta cell replacement therapy for diabetes. In type 1 diabetes, beta cells are mostly destroyed, and in type 2 diabetes beta cell numbers are reduced by 40% to 60%. The proof-of-principle that cellular transplants of pancreatic islets, which contain insulin-secreting beta cells, can reverse the hyperglycemia of type 1 diabetes has been established, and there is now a need to find an adequate source of islet cells.” At this time, the only real hope was using human embryonic stem cells.

Ten years later, in Amsterdam, the research team discovered that, “all acinar and ductal cells – cells that produce digestive enzymes and transport them to the gut – actually contribute to [the] process [of repairing pancreatic cells]. All cells in the pancreas that produce digestive enzymes and transport them to the gut can contribute to its regenerative capacity.”

The initial study was fifteen YEARS ago, and in genetic research, that’s like decades. The work in Amsterdam took place in 2021. Today, researchers in Shanghai, China, “Utilizing the patient’s own endoderm stem cells (EnSCs), they were able to differentiate these stem cells into functional pancreatic islet cells – cells in the pancreas that secrete hormones, including insulin and glucagon, that help regulate blood sugar levels.”

What does this mean? It means the team in China found that they could use…the patient’s own “undifferentiated cells, found throughout the body after development, that multiply by cell division to normally replenish dying cells and regenerate damaged tissues...” All of us have them, they’re what heals the skin or any kind of internal damage we suffer during routine surgery. These stem cells do not depend on the use of fetal tissue. “[researchers] were able to differentiate [the patient’s own] stem cells into functional pancreatic islet cells – cells in the pancreas that secrete hormones, including insulin and glucagon, that help regulate blood sugar levels then transplant them into the patient’s pancreas.”

What happened? “Following a kidney transplant in 2017, the patient experienced a decline in pancreatic islet function, necessitating daily multi-dose insulin injection.” His stem cells were removed and grown, and after they injected them in the pancreas…”the patient achieved insulin independence within a mere 11 weeks post-transplantation. Oral medication for diabetes management was gradually reduced and ultimately discontinued a year later. Follow-up examinations conducted over a prolonged period revealed restored pancreatic function, with the patient no longer requiring insulin or oral or injectable medications that had become in short supply due to their use as weight-reduction drugs. Additionally, normal kidney function was maintained, suggesting a potential long-term cure for both type 2 diabetes and the underlying complications associated with the initial kidney transplant.”

NOTE! The procedure had been successfully attempted on this single patient at the time of the publication of the article in May of 2024. There may be others in the pipeline; but there’s no further evidence of any wide-spread study or a call for volunteers.

What it SHOULD inspire is HOPE. If not for me, then for anyone else in the future who finds themselves facing Type 2 diabetes for a real cure in our lifetime!

Links: https://cells4life.com/2024/05/stem-cell-therapy-achieves-cure-for-type-2-diabetes/, https://nyscf.org/resources/uncovering-the-unique-way-the-pancreas-regenerates/, https://genomemedicine.biomedcentral.com/articles/10.1186/gm277; https://nyscf.org/resources/uncovering-the-unique-way-the-pancreas-regenerates/ Image: https://asploro.com/wp-content/uploads/2019/12/Diabetes-Research_Open-Access.jpg

Sunday, September 8, 2024

GGTA…TYPE 2 DIABETES #24: People Over 65 Have Been EXCLUDED From Diabetic Research!”

For the first time since I started this blog 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!


Dr. Elbert Huang, director of the UChicago Center for Chronic Disease Research and Policy, wrote in April of 2024: “The exclusion of older adults from early [Type 2 diabetes] trials stems in part from the complexity of aging, which can include multiple diseases and medical conditions occurring simultaneously. However, their absence meant the studies essentially did not represent how diabetes presents in the real world. “The majority of people with diabetes are over 65, so our evidence was not based [on data from those people].”

Startlingly, I now find myself in the class of people who have not appeared to matter to the medical establishment. We’ve lost perhaps a decade of time in looking for treatments for older adults who have Type 2 diabetes. How many people – I ask this sarcastically, because what do people who are more familiar with paper letters than cellphones and are usually over 65 REALLY matter in this 5G world [which is, I read, how FAST we get our internet information. (3G was born in 2008 and let us get our data at a rate of 3 megabytes per second. 4G boosted that to 14 megabytes pers second (MBPS). 5G boosted that to 100 MBPS to its SIX AND A HALF BILLION USERS.]

Clearly, not worth talking about.

That appears to be changing. Dr. Huang was of the opinion that “…[to the medical world] the sickest patients should get less medication because they're [un]likely to…benefit from [them]…it goes back to insulin: the original trial comparing moderate and intensive glucose control…was conducted during a time when the number of available drug classes were very limited [ie: no Glipizide, Metformin, Ozempic, or any of the other modern treatments]...that trial showed that people do better with lower blood sugar, but you had to live for at least 10 years to see the benefit.” The subtext there of course, is “and all these old people won’t make it that long, so why bother studying them because NOTHING IS GOING TO CHANGE.

Huang goes on to say, “…cancer and heart disease can disqualify people from participating in [drug treatment] trials. Yet…patients with such conditions are representative of average geriatric diabetes patients, and physicians must be able to treat them.”

Huang concludes: “For many years people have talked quite vaguely about older patients, saying, ‘This older patient is complex,’ ‘This older patient is frail. Now we have tools that are much more specific and reproducible,” Huang said. “And now we can with greater specificity say who is missing from the trials, which could help us reexamine trial data and reshape how we design trials in the future.”

A recent result of this changed attitude led to Mounjaro and Zepbound: “A key study of [tirzepatide, the main ingredient of those two “Brand Name” drugs, discovered that there was] a significant reduction in the risk of progression to type 2 diabetes in adults with pre-diabetes and obesity or overweight…[which] achieved significant results, demonstrating a 93-94% reduction in risk of progression to type 2 diabetes [compared to placebo].”

The implication is that testing the drug on people 65+ discovered that not only could we TREAT Type 2 diabetes, we can now PREVENT it altogether – and avoid the concurrent drain on the cash-payout of the massive profit-driven insurance companies that are required by law to cover us “Golden-Agers”!

Source: https://biologicalsciences.uchicago.edu/news/new-diabetes-drugs-prompt-reassessment-care-strategies-older-patients; https://investor.lilly.com/news-releases/news-release-details/tirzepatide-reduced-risk-developing-type-2-diabetes-94-adults Image: https://www.hcd.com/wp-content/uploads/2021/01/living-well-with-diabetes.jpg

Sunday, August 18, 2024

DIABETES RESEARCH RIGHT NOW! #20: First-Ever Cure for Type 2 Diabetes??? Through Stem Cell Treatment?

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: New research points to using a person’s OWN stem cells to “switch on” genes that could turn it into an insulin-pancreas cell!

The article starts, “Scientists undertook a study centered around a 59-year-old male patient with a 25-year history of type 2 diabetes. Following a kidney transplant in 2017, the patient experienced a decline in pancreatic islet function, necessitating daily multi-dose insulin injections.”


To translate this into English and also give you a framework for this entry:

A guy with Type 2 diabetes who had to get a kidney transplant because his own kidneys stopped working. (You might or might NOT know is that, according to Wikipedia, “Long-term complications from high blood sugar include heart disease, stroke, diabetic retinopathy which can result in blindness, kidney failure, and poor blood flow in the limbs which may lead to amputations.”)

His 25-year-long struggle with diabetes destroyed his kidneys; so, with 21st Century medicine, they found a donor (possibly from his family; possible from a stranger), and gave him a new kidney. But what happened to his ORIGINAL kidney would likely happen again – this time more quickly.

To prevent that and to MAYBE kick-start his own pancreas into making the correct levels of insulin again, they began an experimental procedure that MIGHT start his pancreas making insulin again.

The next bit is difficult even for ME to understand and I have a BS degree in Biology. So, let me see if I can translate it into “normal people” English:

“Utilizing endoderm stem cells (EnSCs)”: using a big needle under sterile conditions, doctors remove these endoderm stem cells…

PAUSE. At one time, the ONLY place to get these kinds of cells was through the use of the embryos of aborted fetuses. That has changed in the third decade of the 21st Century. They CAN use the stem cells that are found in all of us, no matter our age. “‘Induced pluripotent stem cells’” are a type of cell that can be generated directly from a somatic (YOUR body cell) with the introduction of four specific genes. Doctor Shinya Yamanaka was awarded the 2012 Nobel Prize along with Sir John Gurdon “for the discovery that mature cells can be reprogrammed to become pluripotent.”

Not ONLY that, Pluripotent stem cells hold promise in the field of regenerative medicine. Because they can propagate indefinitely, as well as give rise to every other cell type in the body (such as neurons, heart, pancreatic, and liver cells), they represent a single source of cells IN EVERY PERSON'S BODY that could be used to replace those cells or organs lost to damage or disease.

“Since these stem cells can be derived directly from adult tissues, they can ALSO be made in such a way that EVERY PERSON could have their own pluripotent stem cell line. The unlimited supplies of these pluripotent cells could be used to generate transplants without the risk of immune rejection. ***This technology has not yet advanced to a stage where therapeutic transplants have been deemed safe.** They ARE being used in personalized drug discovery efforts and understanding the patient-specific basis of disease. And work continues to make the use of these organs an effective and common procedure.

“The hope is that personalized pluripotent stem cells may one day be able to differentiate these cells into functional pancreatic islet cells – cells in the pancreas that secrete hormones, including insulin and glucagon, that help regulate blood sugar levels.”

Another advantage of using these ‘Induced Pluripotent Stem Cells’ is “to generate germ layer/tissue-specific stem cells from PSCs, which proliferate in vitro and are capable of differentiating into mature lineages, in this case, mature, functioning islets of Langerhans – the cells that produce insulin – because they are developmentally close to the desired mature cell type from the beginning, changing them into insulin-producing cells should be more efficient. Also, their restricted developmental potential provides a system to study various cell-cell interactions during differentiation into insulin-producing pancreas cells.

This treatment is NOT coming to a hospital near you any time soon!

HOWEVER, it IS COMING! Maybe not soon enough for me, but MAYBE soon enough for any of my kids or grandkids should they find themselves in the same situation I am!

Source: https://en.wikipedia.org/wiki/Induced_pluripotent_stem_cell
Links: https://cells4life.com/2024/05/stem-cell-therapy-achieves-cure-for-type-2-diabetes/
Image: https://asploro.com/wp-content/uploads/2019/12/Diabetes-Research_Open-Access.jpg

Sunday, August 4, 2024

GUY’S GOTTA TALK ABOUT…TYPE 2 DIABETES #23: Ozempic, Rybelsus, and Me

For the first time since I started this blog 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’ve started to take the pill-form of OZEMPIC (Which helps control blood sugar spikes and reduces hunger pangs.) …AND “certain people” have leaped on the bandwagon DEMANDING to be able to use the WONDER-WORKING MIRACLE WEIGHT LOSS DRUG THEY CAN INJECT AND EAT ANYTHING THEY WANT AND *POOF!!!* THEY WILL LOSE WEIGHT WITHOUT MAKING A SINGLE CHANGE IN THEIR LIVES!!! AND WHY SHOULD DIABETIC PEOPLE GET TO HAVE ALL THE FUN????)

Anyway, I’ve started taking Rybelsus® because my A1c climbed to 7.7 this last time after holding at 7.1 from 9/22-4/23; jumping to 7.6 in 1/23; dropping to 7.0 on 10/26; and re-leaping to 7.7 on 7/25…

So, besides having to start taking Rybelsus (I DID NOT FEEL LIKE GIVING MYSELF SHOTS!!!), what does all this MEAN?

Let’s start at the beginning.

Both Rybelsus and Ozempic are from a family of drugs called “semaglutides” What precisely does that MEAN in relation to Type 2 diabetes?

So, there seems to be no simple explanation of what a semaglutide is, so I get to do my Translating the Science schtick again! It’s been a while. Hope I’m not too rusty.

Before delving into WHERE it came from, I thought I’d share some startling information with you. So often, I hear about how “AMERICANS” are big, old fat food pigs and that the epidemic of Type 2 Diabetes is caused by our extravagant food-eating and exercise-o-phobic society.

The semaglutide and tirzepatide, which was being developed for the control of Type 2 diabetes SEEMED TO ME to be subsumed by the absolutely INSANE demand for the drugs known as the semaglutides Ozempic, Wegovy, HERS, HIMS, Mounjarno, IVY RX, or the oral, tablet version of semaglutides called tirzepatide Rybelsus, Zealthy, Effecty, and others.

But what do they DO?

From the Mayo Clinic (main HW is here in my home state of Minnesota, in the place my sister and her husband live); “Semaglutide injection is used to treat type 2 diabetes. It is used together with diet and exercise to help control your blood sugar. This medicine is also used to lower the risk of heart attack, stroke, or death in patients with type 2 diabetes, obesity, and heart or blood vessel disease.”

OK, still a bit vague. Let me dig a bit more. First an image:
Then an explanation...
First, the semiglutide is a molecule that MIMICS the effect of a glucagon-like peptide-1 (GLP-1) receptor agonist. Glucagon is “a hormone formed in the pancreas which promotes the breakdown of glycogen to glucose in the liver”.

Glycogen is “a substance deposited in bodily tissues and is a form of “stored” carbohydrates in the liver and your muscles. It’s an ABSOLUTELY INSANELY complicated molecule formed of zillions of glucose molecules. Glucose is the SIMPLEST sugar and THE energy packet that powers EVERYTHING in your body. It is broken down by “hydrolysis”, which happens when enzymes chop up a glucose molecule and release energy and something called pyruvic acid (don’t worry about it here!)

Ozempic, Rybelsus and all the rest are a molecule that MIMICS the effect of a glucagon-like peptide-1 (GLP-1) receptor agonist…

The #&$%@*!!! Does THAT mean????

I thought you’d never ask, because it’s really simple: “GLP-1 agonists are medications that help lower blood sugar levels and promote weight loss.”

YOU probably don’t really want to know what that means, but me being me (a former science teacher and a biology major in college), I DO want to know…

More specifically, an agonist is a chemical that turns on some kind of reaction in a cell when it hooks up with a receptor. The receptor is a molecule on the outside of a cell’s skin that reacts to a particular kind of molecule. When the two hook up, in the case of active ingredient of Ozempic or Rybelsus or Monjarno, or any one of the others, it does a WHOLE BUNCH OF STUFF:

First, it makes your pancreas dump insulin into your blood, scooping up the extra sugar that gives you high blood sugars.

Second, it blocks glucagon – which is out of whack in anyone that has Type 2 diabetes – from telling your liver, “MORE SUGAR! MORE SUGAR!”

Third, it slows how much food gets digested (turned into glucose) and gets dumped into the blood stream, leading to (duh) high blood sugar!

Fourth, it makes your stomach feel full, so you don’t eat so much. If you don’t EAT so much, there won’t be so much food being digested, and there won’t be as much glucose released into your blood.

So– now that I UNDERSTAND what Rybelsus does to my insides; what Ozempic used to do to my wife’s insides…I can take the (stupid…but LESS stupid now that I know what my meds do…) meds to keep me from getting all the other crap I can get if I don’t try and get my diabetes under control…

The drugs are to HELP ME do something I can’t do anymore. Get it? Got it? Good! (

Saturday, July 13, 2024

ALZHEIMER’S RESEARCH RIGHT NOW! #19: Slowing Down Alzheimer’s!?!?!?

From the first moment I discovered my dad had been diagnosed with Alzheimer’s, it seemed like I was alone in this ugly place. Even ones who had loved ones suffering in this way; even though people TALKED about the disease, it felt for me like they did little more than mumble about the experience. Not one to shut up for any known reason, I added a section to this blog…My father passed some years ago, so the immediacy of Alzheimer's has waned. However, research continues. VERY sporadically, I’ll be highlighting Alzheimer’s 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. ALZHEIMER’S RESEARCH RIGHT NOW! #19: Slowing Down Alzheimer’s!?!?!?!?!

From the first moment I discovered my dad had been diagnosed with Alzheimer’s, it seemed like I was alone in this ugly place. Even ones who had loved ones suffering in this way; even though people TALKED about the disease, it felt for me like they did little more than mumble about the experience. Not one to shut up for any known reason, I added a section to this blog…

VERY sporadically, I’ll be highlighting Alzheimer’s 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:
“FDA Approves a Second Alzheimer's Drug That Can Modestly Slow Disease” PLUS “First-of-its-kind test can predict dementia up to nine years before diagnosis”

“Researchers at Queen Mary University of London have developed a new method for predicting dementia with over 80% accuracy and up to nine years before a diagnosis. The new method provides a more accurate way to predict dementia than memory tests or measurements of brain shrinkage, two commonly used methods for diagnosing dementia.”

“U.S. officials have approved another Alzheimer’s drug that can modestly slow the disease, providing a new option for patients in the early stages of the incurable, memory-destroying ailment. The Food and Drug Administration approved Eli Lilly’s Kisunla…for mild or early cases of dementia caused by Alzheimer’s.”

DO YOU SEE THE POSSIBLE SIGNIFICANCE OF THIS???

IF doctors and scientists are able to consistently predict dementia using fMRI scans from 1,100 volunteers taken from a UK database holding a half a million participants. From that study, they can then estimate the strength of connections between ten regions of the brain that make up the most significant parts of the brain.

After they figure out that I’m a candidate for developing Alzheimer’s, they should be able to the new drug to slow the disease SOME during the early stages of the disease – more specifically “for mild or early cases of dementia caused by Alzheimer’s.”


While no use for Dad, and ALSO given that knowing that I had/have a sporadic fear that with my dad diagnosed with Alzheimer’s I’m more likely to be diagnosed with it ANY DAY NOW!!!...

Yeah, I know, my own brain drives me crazy sometimes! (OH! “Crazy” is not the same as “Alzheimer’s”!

Finally, I searched and found this: “…statistics related to the risk of developing Alzheimer’s in your lifetime digs up some 3 million hits from Google!

I COULD pore over them and feed my fear, or I could accept the reality that if I’m 60 years old today (I’m currently 67) the odds of developing Alzheimer’s are 4.8%, or in other words, there is a 95.2% chance that I WON’T develop the disease.”

You (like me) might as, “is that a general chance or does it include people whose parents were diagnosed with Alzheimer’s?” The research reaches the following conclusion, “If you have a first-degree relative with Alzheimer’s disease (e.g. mother, father, sibling), your risk of developing the illness is about two to three times higher than someone else your age who doesn’t have a family member with the illness.”

OK – that seems straightforward. That puts my chance of developing Alzheimer’s at (using 2.5 times 4.8 = as likely) at 12%. That’s two chances in twenty-five or about one in twelve; twelve and a half to be precise. So, if we put twelve and a half people in a room, I will have Alzheimer’s, eleven others will not, and there will be a grisly murder for someone like Hercule Poirot to solve. (Which, being in a writing state of mind, puts an idea into my head…)

So, I live in the decade where it has become to not ONLY figure out if I’ll develop Alzheimer’s, it’s now possible to TREAT that diagnosis.

While I’m certainly not immune, I can add to the reasons that it’s unprofitable to worry about being diagnosed with Alzheimer’s. I hope it helps you as much as it quieted my own heart; ‘cause it helps a bit.

Resources: https://www.sciencedaily.com/releases/2024/06/240606152250.htm,https://www.usnews.com/news/business/articles/2024-07-02/fda-approves-a-second-alzheimers-drug-that-can-modestly-slow-disease
Image: https://www.charities.org/wp-content/uploads/2023/10/ADR.png


Sunday, June 30, 2024

DIABETES RESEARCH RIGHT NOW! #19: After Fasting, Why the @!&%$ Are My Blood Sugars STILL Through the ROOF???

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: “One of the most confusing aspects for patients with type 2 diabetes is that we have high fasting glucose levels.” So – WHAT’S THE ANSWER???


“The World Health Organization (WHO) considers type 2 diabetes, one of the pandemics of the 21st century…it is a condition that results in high levels of circulating glucose -- the cellular energy fuel -- due to a deficient insulin response in the body…When blood glucose, also called blood sugar, levels rise after you eat, your pancreas [is supposed to] releases insulin into the blood. Insulin then lowers blood glucose to keep it in the normal range…In T2 patients, the glucose synthesis pathway in the liver (gluconeogenesis) is hyperactivated, a process that can be controlled by drugs such as metformin. ”

But metformin has never CURED T2. It wasn’t meant to. It’s a way to CONTROL T2. This group of researchers noticed something odd. From the beginning of the COVID 19 pandemic, “…factors involved in the control of gluconeogenesis [which is the liver making blood sugars and injecting them into our bloodstream]… sometimes patients hospitalized with COVID-19 showed high glucose levels…[it] seems to be related to the ability of the virus to spark the activity of proteins involved in starting the liver up making glucose and sending it to the bloodstream…”

So, that response of the bodies of people with COVID sometimes made their body react as if they were also Type 2 diabetic. Now, I take FOUR metformin tablets every day. I was SHOCKED to read this: “The mechanisms of action of metformin, the most commonly prescribed drug for the treatment of type 2 diabetes, which reduces how much glucose is in the blood, are still not fully understood.”

In other words, researchers, doctors, and pharmacists DON’T KNOW HOW METFORMIN WORKS!!!!!!! While I intentionally made that more alarm than I could have, the fact is that as researches dig into the method of metformin function, they’re finding out WAY more than they expected, up to and including the effect of metformin in REDUCING AGING!!! “Early evidence highlighted the liver as the major organ involved in the effect of metformin on reducing blood levels of glucose. However, increasing evidence points towards other sites of action that might also have an important role, including the gastrointestinal tract, the gut microbial communities and the tissue-resident immune cells.”

“At the molecular level, it seems that the mechanisms of action vary depending on the dose of metformin used and duration of treatment. Initial studies have shown that metformin targets hepatic mitochondria; however, the identification of a novel target at low concentrations of metformin at the lysosome surface might reveal a new mechanism of action. Based on the effectiveness and safety records in T2DM, attention has been given to the repurposing of metformin as part of adjunct therapy for the treatment of cancer, age-related diseases, inflammatory diseases, and COVID-19.”

Rest assured, I’ll be poking around this paper more as time goes on!

To briefly recap, it seems that HOW metformin works is even deeper than just at the level of CELLS – but deeper still into the “powerhouse” of every cell in your body: the mitochondria…

So, that’s it for now. Obviously I’ll continue to dig deeper into HOW metformin works. (I commented to my wife with a sigh, “Oh, great, now metformin with become as hard to get as Ozempic because the rich will start to pop the pills to stay young and beautiful!”

*sigh* I vote we should just suppress THAT little bit of information!

Links: https://www.sciencedaily.com/releases/2024/06/240607121434.htm; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214027/; https://fagron.com/news-media/post/exploring-the-multifaceted-benefits-of-metformin-hydrochloride-beyond-diabetes-management/ ; https://www.nature.com/articles/s41574-023-00833-4