Canagliflozin (mixed SGLT1/2 inhibitor) did NOT prevent 18oz blueberries from spiking my BG briefly to 182… (this is the highest I’ve ever seen it)…
Fuck all the misinformation on the Internet about blueberries and glycemic control, even other fruit doesn’t spike it this high.
Where did you source your canagliflozin?
I often eat oatmeal with walnuts and blueberries for breakfast and canagliflozin works for me. Never have I seen a spike over 120 for any meal immediately preceded by canagliflosin.
Berries are definitively a very healthy thing to regularly consume. Consumers have access to data they’d never have had prior due to CGMs.
The take away message here isn’t that blueberries or fruit are bad. I’m not even that excited as a physician about someone having a spike of blood glucose that is brief with underlying longer term average consistent with a HbA1C goaling ~4.7-5.0.
If one is worried about getting a spike - wear a CGM and test different foods in isolation - and be aware of foods that will generate a significant spike. Each individual is different in what type of spike they’ll get with a given food.
For items that generate a significant spike, don’t eat them in isolation - have your fats, proteins and more complex carbs first then add the items that are healthy and in isolation generate a spike, last, once the other stuff is percolating in your stomach.
The area under the curve and the spike is almost always minimally affected by the offending food that in isolation would have generated a spike, when having other foods already in your stomach that slow absorption.
What brand of canagliflozin is this that you are using?
Honestly, I’d go with empagliflozin or dapagliflozin over canagliflozin. I wish the ITP would test empagliflozin or dapagliflozin.
Another paper just published in Neurology: Sodium-glucose Co-transporter 2 Inhibitors Lower the Risk for Dementia in Patients with Type 2 Diabetes Mellitus
Patients with T2DM on SGLT2i presented with a significantly lower risk of new-onset dementia (HR: 0.56; 95% CI, 0.54–0.57), VaD (HR: 0.58; 95% CI, 0.54–0.61), AD (HR: 0.52; 95% CI, 0.49–0.54), FTD (HR: 0.68; 95% CI, 0.55–0.84), and DLB (HR 0.50; 95% CI, 0.42–0.60) compared to patients with T2DM on DPP4i.
It’s again massive and across all dementia subtypes. 
This literature is part of my database that keeps growing in support of this class of drugs.
T2DM in and of itself increases risk of AD. So it is somewhat speculative as to whether an SGLT2-i would make even a bigger decrease in Relative Risk of AD or less of a Relative Risk Reduction in non diabetics. I could see an argument either way.
Our other groups of patients who take these agents on label already have other significant disease, that I’d expect to pre-dispose to dementia.
Looking at healthy individuals who get randomized to these agents would be a great study. I doubt it is forthcoming as there just doesn’t seem to be a focus on longevity - only disease treatment. Funding a study in this area by industry would have a great financial argument as demonstrating longevity or decreased AD in healthy individuals or better yet in E3/E4 and E4/E4 individuals would yield a drug that virtually everyone as they get older might want to pursue.
I believe that you should not think of T2D as a certain point at which anything above is diabetic and everything below is fine. I believe that we are all diabetic to some degree. Therefore SGLT2i will be beneficial to all to some degree.
Especially as I see my blood glucose levels going up every year.
The above paper shows that SGLT2i slash the risk of dementia by 2 in people with T2D compared to DPP4! So the potential neuroprotective effect is probably not related to the glucose-lowering properties of SGLT2i.
Also, SGLT2i are approved in people without diabetes for CKD and HF (and probably soon for cardiomyopathy, NAFLD, and atrial fibrillation). I hope that researchers will look at dementia outcomes in these populations as well.
We simply don’t know the size of effect on healthy individuals without these underlying health issues, where we see decreased AD incidence in patients who due to the indications for taking an SGLT2-i are already at elevated risk of getting AD.
I have some patients with T2DM, but have more who have an ApoE3/E4 or E4/E4. I wish there was better data on use in the context of decreasing risk of AD in individuals who have elevated risks, but don’t have any of the current indications for these drugs.
it was agelessrx’s canagliflozin
" For items that generate a significant spike, don’t eat them in isolation - have your fats, proteins and more complex carbs first then add the items that are healthy and in isolation generate a spike, last, once the other stuff is percolating in your stomach."
I ate 2 beyond meat patties (the avocado oil ones) prior to the blueberries
Oooh nooo 
"Unfortunately, even though an alternative to beef is better for the environment, it may not necessarily be better for your health.
The Beyond Meat burger has 18 ingredients, the Impossible Burger has 21. Both are highly processed and contain several additives and inflammatory oils.’
Were you on the full dose for several days in a row so you built up to full normal exposure? Or were you just doing the half pill every other day or something?
“The Beyond Meat burger has 18 ingredients, the Impossible Burger has 21. Both are highly processed and contain several additives and inflammatory oils.’”
why are the oils inflammatory? Source of it?
I saw the avocado oil one for the first time and had to try it to see what it’s like. Idk if I’d try it frequently again.
I’ve been in empagiflozan 10 mg for several weeks now (purely for longevity/health span; A1c is 5.4; hope to bring it down to < 5) and can still get big spikes, e.g if I eat sugary dessert. But as this thread has shown, as well as the other threads on sglt2i’s, there is way more to these drugs than decreasing spikes. The same can be said for acarbose.
Our analysis shows that SGLT2 inhibitors likely improve adipokine biomarkers and insulin sensitivity, but there is little evidence that SGLT2 inhibitors improve other inflammatory biomarkers including CRP.
Effect of sodium glucose cotransporter 2 inhibition immediately prior to heart transplantation 2024
Guidelines suggest withholding SGLT2i preoperatively due to the risk of ketoacidosis. Orthotopic heart transplantation (OHT) occurs without sufficient notice to cease SGLT2i treatment before surgery. In a retrospective analysis of 163 OHT recipients (40 exposed to SGLT2i, 123 not exposed), we show no increase in rates of mild, moderate, or severe acidosis postoperatively. No cases of ketoacidosis occurred, likely due to the fact that 97% of patients received insulin infusions postoperatively for transient postoperative hyperglycemia. Patients exposed to SGLT2i had shorter length of stay in the intensive care unit and improved adjusted survival overall.
Great!
Fuck all the misinformation, period!
Yeah, well, do you really think avoiding it will have an effect, marginal at best, unmeasurable compared to the best interventions.
Probably, no worse or better than regular meat.
You must have gotten the latest version.
“In February 2024, Beyond Meat announced plans to switch from canola and coconut oils to avocado oil in its Beyond Burger patties and Beyond Beef grounds. The new beef products will also have less sodium and more protein.”
I’m doing a 5 day fasting-mimicking protocol (PROLON) next weekend and considering whether I should stop my empagliflozin (25mg) before then. There’s a risk of ketoacidosis with surgery and true fasting, but since I’ll still be eating 3 low calorie meals per day (each of which actually contains carbs) that this risk should be minimal to none. Does anyone have any thoughts or experience w/SGLTi and fasting or FMD?
Maybe because empagliflozin specificially protects renal function while at the same time (indirectly) causing a higher metabolic rate?