I definitely feel the need to be warmed up 30 minutes or much more. Oddly, my body feels more primed and ready for a hard cardio workout when having expended calories for a long period of time (versus when younger). My conjecture is that my mitochondria aren’t ready until they have been exposed to some sort of zone 2 training for a period of time. With strength training, I seem to transition pretty smoothly into my reps without extensive warming up.
I agree HIIT is time consuming 
It could actually be that it is not “corrected for insulin” resistance but that regular spikes does lead to increased risk of insulin resistance.
Or that even in a non insulin resistant person (or mouse) it is still not good for longevity to increase insulin secretions and that is what happens each time blood glucose goes up.
That insulin could be bad in many ways for longevity could be part of how other growth pathways (mTOR, IGF-1, high T / Free T, etc) are massively bad for longevity.
Btw, absence of evidence if not evidence of absence.
So when you state “I can see no clear evidence that spikes after meals can be harmful” that does not mean that a longevity optimizing person should feel that they can or should ignore spikes.
Rather without black and white evidence we still need to do the best we can and still weight
all the reasons why it “could” be bad even if we don’t “know” and then trade that off agains all the reasons it might be bad (whether there are risks, costs, effort) to avoiding the thing (in this case spikes). (And of course weigh the strength of support for each type of information, data, mechanistic rationale, etc)
For me personally, is seems that this is a very asymmetric trade off that clearly lines up that it’s worth the trade-off to seek to generally avoid blood spikes as it may be (or in my view likely) is a more pro longevity behavior.
For instance I’d need evidence that the glucose spikes *are not”
While Levels does have an incentive and you should review what they say with skepticism, the underlying sources they cite/link to might be helpful for you (see further below)
Also looking at the logic in how Peter Attia feels that spike and variability is negative might be helpful:
Levels
What glucose reading after a meal is considered a glucose spike?
@LaraPo, I’ve personally been aiming for an increase in blood glucose of less than 30 mg/dL at 1-2 hours post meal compared to the premeal reading. I’m not a doctor so you may get better input from someone else of course. I took a course this year called data driven fasting and that was the recommendation we followed to determine how to eat to avoid large glucose spikes. As I understand things it’s somewhat individual with different amounts of food, types of food and macro splits having varying impacts depending on the person. I was not in a good place diet wise when I started rapa due to numerous food sensitivities/intolerances. Rapa seems to have resolved most of that (Thank God) but in the process I had to learn how to strategically manage reincorporating foods I hadn’t consumed for years without becoming diabetic! I’m looking forward to learning and improving more but in the meantime I’m continuing to regularly check my glucose.
I read that if Acarbose is started at 16 months in mice, it seemed less effective than Rapamycin alone. Is that correct?
Hi, and welcome to the forums. yes - acarbose is less effective the older you get (at least in mice). Details here: Acarbose - Details On Another Top Anti-Aging Drug
Thank you, I appreciate that you sent the links, and sharing your line of thinking about this . Originally I asked about evidence/references for postprandial blood sugar spikes per se being harmful in healthy people, in this thread. And I agree: Nobody needs high blood sugar peaks in their day to day life. In other words: There is no clear advantage to having these blood sugar peaks, so why not try to minimize the spikes?
If one has a crappy diet and then decides to change the diet according to one parameter only: lower postprandial blood glucose, then sure, that will undoubtedly lead to better health outcomes since a lot of the food that has a high glycemic index is of low quality in many other respects. But lets say you have a diet that includes a decent level of vegetables, fruits, berries, animal foods and very little ultraprocessed foods, and little processed foods. Will a change from a fair amount of potatoes, rice and other high glycemic foods in that diet to for instance low glycemic beans and lentils change anything?
The links you sent do not address that question, as far as I can see.
Insulin is related to glucose spikes, but consuming low glycemic index meals do not appear to give lower IGF-1 than high glycemic index meals, postprandially: Glycemic load effect on fasting and post-prandial serum glucose, insulin, IGF-1 and IGFBP-3 in a randomized, controlled feeding study The fasting IGF-1 was reduced after the low-GI-diet, but this, again, can be related to a range of other diet quality factors.
Non UPF high carbohydrate foods are typically lower in AGEs than foods that contain more protein and fat, so even though you might get lower amounts of endogenous AGEs with a diet that aimes at reducing PPG, what is the total sum of the preformed diet AGEs and the endogenous AGEs in any given diet? And there are many more questions such as these. And we can get sidetracked with the details, and bends and turns here, but my main point was that I am looking for mechanistic or clinical studies that elucidate better the effect of postprandial glucose peaks in its own right, and not as a proxy for diabetes, insulin resistance, a low quality diet or other aspects.
An asymmetric trade off for me and my patients would be to advice people against potatoes for dinner in exchange for more meat or legumes for instance. The upside of not limiting potatoes appears larger than the possible downsides given the evidence. Especially if you really like potatoes, and don’t get that much vitamin C from other foods for instance. So this is not about not erring on the side of caution or that one should wait with doing something in spite of there not being clear evidence.
This is an area of interest for me given my genetic predisposition toward t2d. I am not certain that blood sugar “spikes” are damaging but I try to avoid adding to the problem by:
(1) eat a lot of fiber at every meal, in part to slow digestion of carbs
(2) eat some fats and protein before eating carbs, to slow digestion of carbs
(3) exercise immediately after eating high carb foods, such as apples
(4) almost never eat added sugar or highly processed starches (bread, pasta)
(5) new: exercise zone 1 (easy) to start the day and end the day to lower cortisol (lower adrenaline—> lower blood sugar)
It’s an important course to take! I also would love to understand more about food intake and glucose changes. The normal fasting (10-12 h) range is from 70 mg/dL to 100 per Google 
. Hyperglycemia is when it spikes higher than 180 mg/dL after a meal. Mine is never higher than 130 mg/dL after a meal. My fasting glucose when on Rapa is 90-94 mg/dL, when off Rapa it’s below 90.
30 mg/dL seems abnormally low. Are you sure it’s the right number?
FWIW
She’s saying the difference between fasting and post-meal is 30. So if fasting is 90, then post-meal would ideally be less than 120. Hard to do if you like food.
In a few days I am meeting with my cardiologist and asking or “demanding” to be put on a PCSK9 agent. The doctor failed. in my opinion, to aggressively lower my LDLs, even though I have Hx of stent 10 years ago, with only statins on board, and now with 50% or more closures of coronary arteries. Get your LDL to 20. Get an MD who will work with you aggressively and proactively. I know it is difficult to change to a new MD but you have only your life to lose…
I think there are several possible routes to reducing plaque. As usual the most likely to work are also the most expensive and difficult.
Nattokinase, I started on 12000fu after my latest bad CAC. We have one paper, and my brother as evidence. Not great but the downside is very small. Somebody found a 6000, I need to find it again.
Alpha and beta cyclodextrin. Not much downside here either, but the beta is a pain in the butt. Pun intended.
IV phosphatidyl choline. Apparently this helps dissolve the cholesterol. Expensive and not sure how effective. I did read a paper, don’t have it with me now, but can find if you like.
Chelation. This is a long shot. I have an appointment to an infusion center. They are going to give me a 3 hour infusion of EDTA, following that you collect urine for 6 hours to see if you have any heavy metals. This is called a challenge. I have no evidence this could work at all, but seems scientific. $180 for the EDTA, $80 lab fee for the urine. Good way to find out if chelation may work maybe?
People with low LDL can still have a heart attack and still build plaque. Heart attack and stroke are both caused by a blood clot. I’m not a doctor.
You’re in charge of your health. Good luck,
https://www.metabolismjournal.com/article/S0026-0495(23)00244-5/fulltext
" Sasso et al. [2004] showed a linear relationship between post-load plasma glucose levels in patients with normal glucose tolerance and the number of stenosed coronary arteries at angiography [
[41]
]. This supports the concept that post-prandial glucose levels are an independent risk factor for cardiovascular disease, exerting a greater effect than fasting or baseline glucose levels [
[42]
]. Mortality data from nearly 20 years of follow-up has shown that individuals in the highest quintile of two-hour post-prandial glucose response had a risk of mortality of 2.7 times that of individuals in the lowest quintile [
[43]
]. Similarly, Oesterle et al. [2022] demonstrated an association between PPHG and the risk of developing heart failure [
[44]
] and Brutsaert et al. [2016] identified a link between PPHG and an increased Atherosclerotic Cardiovascular Disease risk score (ASCVD) [
[45]
,
[46]
].
@LaraPo, forgive me. I meant that I try to keep my post meal glucose from rising more than 30mg/dL above my premeal level. If my premeal is 86 for example I look for a post meal blood glucose of no more than 116. I’ve found it works well for me to track and learn how my body responds different meals.
There is a different metabolism for glucose over around 8mmol/L (144) that may be part of this.
I see now. Thank you. @blsm The difference between 2 readings has to be taken into account! It means that I have to try harder to lower my post meal reading.
Are you waiting couple hours after meal to measure it?
Polyol pathway?
Creates extra ROS. Shouldn’t be a problem unless the body can’t clear it. Keep glutathione levels up. If glucose is high all the time, then bad things are accumulating.
For people like me who are vulnerable to increasing problems with blood sugar, how do I build better metabolic flexibility? Instead of avoiding the need to deal with glucose, how do I improve my body’s ability to deal with glucose?
I think so. It is the reason why we want to keep post prandial glucose at the lower level. I posted my charts which indicated that I had managed to reestablish the lower limit on a post prandial basis.
All of this is about systems not working. I have written a bit more on my page about methylation as I have thought further about it. (down the bottom of the page)