Maybe in the future it will be possible to manage a person's glucose and related hormone levels in roughly a continuous keto or borderline low blood sugar state using the equivalent of an "insulin pump" and a real-time blood glucose monitor control system such that it doesn't promote low-blood sugar neurological symptoms.
That’s already the concept of insulin pumps. The problem currently is that subcutaneous insulin takes too long to work to be very precise, and also, pumps don’t have a concept of carb intake. They try to predict whether automatic doses are need based on trends. Also, typical blood glucose for a non-diabetic person is 85 mg/dL. This is fairly close to the line of hypoglycemia, which is under 70, so automated pumps aim to keep glucose somewhat higher. For the Tandem T:Slim, it attempts to maintain 110, for instance. I am not familiar with most of the drugs listed there but I suspect their action would be far too slow to work very well in that regard.
I have Type 1 Diabetes (T1D) and use a semi-closed loop system, which includes the Libre 2 sensor with XDrip and the Omnipod Dash, managed by AAPS.
AAPS (unlike the Tandem T
, which I’m less familiar with) uses a more sophisticated algorithm to calculate the required insulin, considering several factors:
- Blood sugar levels received via XDrip from the Libre 2 sensor.
- A profile that includes:
- - The basal rate per hour for each time slot
- - The insulin-to-carb ratio
- - The target blood sugar range
- Automatically calculated insulin sensitivity.
- Insulin on board (remaining active insulin), calculated using a curve to estimate how much insulin is still active after injection.
- Carbs on board, with AAPS tracking active carbs over time.
I've heard that AAPS is more sophisticated. I'm definitely not too happy with the Tandem system. Some people say they get better levels with Control IQ, but I don't. The T:Slim does have the ability to set basal rates for different times of day, and takes as input your insulin to carb ratio, correction ratio, weight, and tracks IoB. I don't think the insulin on board algo is very good... it starts decreasing before I see any effect on my glucose, and dissipates quicker than I expect. They base it on insulin lasting 5 hours, I think, but it seems to calculate less time. It's not a 'learning' algorithm either afaik.
The lack of carbs is perhaps the worst for me. Even if I track then on the Dexcom app, it doesn't use them. The automatic boluses are often wrong. When I had it anywhere near my real ratio, it would 'predict' I was going over 160 and automatically dose me. So, say I was at 85, and had 15 grams of potato chips. My glucose would rise quickly and as it went over 125, 140, the system would predict it was going up past 160 - or who knows, since it doesn't know how many carbs I ate. So then it would dose me with say, 1.1 units, which was enough to take my glucose -back to 85-. That sent me in loops a couple of times... 85, eat, up to 145, automatic bolus, back to 85, eat, up to 145 - very annoying when it happened at night. I had to set my carb ratio so high that the automatic boluses are now insignificant amounts like .16 units. It also doesn't notify you on your phone about automatic boluses, which has caused me major problems when I'd also manually correct. The automatic basal reduction (Basal IQ) is useful though.
Anyhow, I'd love to try AAPS but I don't have an Android phone. I also used to follow someone on Twitter who was developing his own software that he said removed the need to pre-bolus at all. Not sure about the details though.
I switched from iOS to Android for AAPS ( i didn't want to carry two phones )
With AAPS - it is usually able to deal with my blood sugars at night automatically.
During holidays ( 0 stress day), AAPS can almost completely determine boluses just based on my profile and carb intake. ( i.e. I don't force a bolus )
However, during normal workdays, I usually need to bolus right before carb intake. AAPS also allows you specify bolus a percentage and then let it figure out the rest automatically.
We could, I guess, with some biochemical wizardy. Insulin does more than just reduce blood glucose, though. It allows the glucose to enter muscle and brain cells to be used for energy. People with Type 1 need just as many carbs and as much energy as other people, of course, it's just that their body can't use it properly. Insulin does have the drawback of being a fat storage hormone though. Such a device sure would be great for people who indulge in too many carbs!
People in ketosis actually have higher fasting blood sugar than those on high carb diets- there is an adaptive insulin resistance that preserves glucose for the brain and heart cells that can’t survive without it.
That said- it is an adaptive mechanism that is rapidly reversible, and totally different from type II diabetic insulin resistance.
The smarter way to look at it: Diabetes increases the chances of dementia. It's diabetes that's causing an unnatural increase. Rhe drug is simply a catalyst for something closer to normal. Obesity at it's current rate, while socially normalized, is from an evolutionary standpoint abnormal.
The article mentions that this effect was seen in only the cohort taking one of two prevalent diabetes medications.
For your interpretation to be accurate, you’d need to also show that the other popular medicine doesn’t work for diabetes type 2 treatment.
FWIW, the last line of the article is a dismissal from a UK doctor saying that this would make the diabetes drug better than any existing Alzheimer treatments, and suggesting that there’s a confounding variable in the study instead.
"For your interpretation to be accurate, you’d need to also show that the other popular medicine doesn’t work for diabetes type 2 treatment."
This is not true. It's possible that there are multiple effects of type 2 diabetes, with multiple drugs that treat the main factor (sugar levels), but with a subset of the drugs affecting other factors (hormones, cellular activities, something else) that influence dementia.
I had read that too, but while those Alzheimer’s teams pivot over the next 10 years for their new research and drug approvals, the thing that treats insulin and glucose processing helps prevent diabetes and dementia
No actually, I'm not. Instead, my baseline is the historic norm, the evolutionary norm. I don't jump to the conclusion of normalizing diabetes and then come up with some throw-more-pills-at-it theory.
In other words, how effective is this "cure" vs no diabetes at all? *That* is the question.
From an evolutionary standpoint, animals cycle from obese to slim year round. Obesity is normal in autumn. Being slim is normal in spring/early summer. Food state wise we are in a eternal autumn.
We are not defending obesity, we are advocating for a balanced view, while you are busy with your little crusade.
My suggestion is to look at old black/white tribal photos of natives. They do not fullfill your beauty standards, but they lived normal sustenance lifes.
And yes, the woman and men have bellies. Not huge ones, but noticeable ones.
Same thing in the animal kingdom.
The dominant monkey in a harem, besides the normal hormonal dominance meat-mountain bloat, usually has a belly.
Our beauty standard is met by animals in distress, being pushed into marginal territories. Healthy is, somewhere in the middle, not on either side of the isles of madness.
If you are overweight, you need to take responsibility and change your lifestyle.
Of course, everyone instinctively knows this even if they want to use mental gymnastics to explain why it is OK. Alcoholics, drug addicts, etc are defensive too and have many excuses at the ready for why their behavior is acceptable.
In the end, however, reality will hit hard and five dollar words aren’t going to save the obese and those with unhealthy lifestyles from sickness and early death.
Not true. Bears live about 25 years. 35-40 years in captivity. I don’t think they’re normalizing obesity upthread, they’re merely pointing out that in nature accumulation of significant quantities of subcutaneous and visceral fat is normal, as are periods of starvation that we no longer experience.
Correct - I wasn't trying to normalize obesity upthread, at all.
Bears are an example that shows very clearly it's normal for animals in nature to become very much "not lean" to survive, and the drive to put on fat stores is probably much broader in nature than animals that hibernate to survive winter.
What's unique about humans is that we've engineered our environment to the point that most of us no longer suffer long stretches of being unfed or underfed to strip the excess fat stores off of us.
Some people are clearly better than others at fighting the behavior evolution has programmed into them. It's not good for them today, but at the same time that drive for survival is what kept their ancestors alive.
Of course we don't, but then again I think bears were just thrown in as an (extreme) example. As I read the thread before that, the point was that most animals' weights vary on an annual cycle, fattened up during summer-autumn and slimmer after the winter. Which seems fairly uncontroversial to me.
From an evolutionary standpoint, like bears, we only managed to survive long enough for our offspring to have offspring, which is all that matters for evolution.
I never understood why these references are being made regarding health.
Bears aren’t healthy. Bears don’t live long. Ancient people weren’t healthy, their diets weren’t healthy and they had lots of untreated issues as well.
I supose quite a few bears live quite long lives -- for being bears.
> Ancient people weren’t healthy, their diets weren’t healthy and they had lots of untreated issues as well.
As far as I've gathered from (pop-sci summaries of fairly recent-ish) research, people in prehistoric and pre-agricultural hunter-gatherer societies were on average at least as healty as -- and often healthier than -- people in later agricultural societies, from the Bronze and Iron Ages through antiquity, the Middle Ages and Renaissance, up until at least the early Modern Age and quite possibly through to our days of (relative, unequally-distributed) affluence and its concomitant recent global obesity.
This only really applies to some animals which developed in moderate climate.
Most primates including us humans are tropical and subtropical creatures, which didn't face classical winters until relatively recently. The Neanderthals did, for a considerable amount of time, and their physiology might have been different, but the Neanderthals were also developed enough to protect themselves using clothing and shelters, and possibly store food, so physiological adjustments might not have been necessary.
Modern humans are basically Africans adapted to ~ Kenyan climate, though. (Yeah I know about the Neanderthal and Denisovan admixture.)
The smarter way to comment online: Read the article before commenting on how to best understand it. As the other reader mentioned, that's not what the article says.
That is, the medication doesn't improve anything per se. The problem is obesity and diabetes. The medication does not perform better than these not being present at all.
The presume diabetes - sans T1 - is a norm is false if not dangerous. In other words, "Sure just throw more meds at it" is not a narrative anyone should be comfortable with.
Diabetes is a debilitating situation. A slow killer. It is an independent factor for both degenerative (Alzheimer's) and vascular dementia. I do not think any drug will be better than the disease itself.
On the other side, if we use a diabetes drug to cure dementia in non-diabetes patients, we might have a good result but with hypoglycemia as a side effect.
For non-diabetics this is fairly easy to prevent (at least it is for me). You just eat a moderate amount of food before taking it (referring to metformin).
DPP-4 drugs are less effective also on other metrics. Would be far more interesting to see the comparison of SGLT-2 inhibitors vs GLP-1 agonists.
For some reason GLP-1 drugs are not that popular in Korea (and still not prescribed just for the weight loss), so that may explain why these researchers haven't done that.
Considering that Alzheimers itself is considered type 3 diabetes and Dementia is heavily correlated, it isn't that surprising.
My own PoV is that a lot of it comes down to the massive increase in heavily refined foods and seed oils in the past century and a half. You have a lot of carbs and a really different mix of fatty and amino acids. So higher blood glucose, more of the time combined with a very different mix of fatty and even amino acids in the diet. Likely exacerbated by half a century of low-fat, low cholesterol diets perpetuated largely in busted myth. Combine this with hyper-palatability and it's just hard to get away from.
Heart disease, alzheimer's, dementia, diabetes, obesity... All of it comes down to food and exercise. With a bit more exposure from RFKjr, it's ironic that Time magazine is now doubling down for the conglomerates, can't find the cover photo for this, but the recent article on why ultra-processed foods aren't that bad is astounding.
- SGLT-2 inhibitors: canagliflozin, dapagliflozin, sotagliflozin, bexagliflozin
- DPP-4 inhibitors: sitagliptin, saxagliptin, linagliptin
Other beneficial drugs beyond/with/for diabetes and/or weight:
- Metformin
- AGIs: acarbose
- GLP-1 agonists: tirzepatide, semaglutide, liraglutide
- DACRAs: cagrilintide
Maybe in the future it will be possible to manage a person's glucose and related hormone levels in roughly a continuous keto or borderline low blood sugar state using the equivalent of an "insulin pump" and a real-time blood glucose monitor control system such that it doesn't promote low-blood sugar neurological symptoms.