#71

By fasted I mean I run in the morning and I don’t eat before. I’m not talking about a multi-day fast which would be totally different.

In my case even though I’m eating low carbs, I do have plenty of glucose in my blood. Too much in fact.
All the zone 2 running has made me super efficient at fat burning and when I run in zone 2 I don’t use much if any glucose and my glucose blood level stays stable.

When I run faster than zone 2 and I start to also burn glucose, my liver makes plenty of it. Too much actually and I see the glucose plunging then rising up above the already elevated starting point.

BTW according to my Stryd, my running power was above 400W for 36s for my 200m sprints.
That’s 14000 J = 3.3 kcal. Carbs are at 4kcal/g so that’s 0.825g of carbs if I only used carbs during that run.

The total session used 403 kcal according to my Garmin watch but most of it is the zone 2 warm up, recovery and cool down which are not really using carbs.
My ketones did not rise either.

Really no need to eat carbs before an HIIT session.

1 Like
#72

Can I ask are you using 10mg or 25mg Jardiance?

#73

I am using 10 mg. I would try it for at least 30 days before switching to 25 mg if 10mg doesn’t give the result you want.

2 Likes
#74

@desertshores What results are you looking for with Jardiance? (I take 12.5 mg)

#75

As an aside, I am having unexpectedly good results from Jardiance. I am taking Jardiance alone because because like regular milk, metformin no longer agrees with me. The Jardiance alone has brought my fasting glucose levels to 85 - 95 mg/dL.
I eat a low carb diet. It took about a month for Jardiance to bring my levels below 95.
I also take Acarbose before any meal that is not low carb.

4 Likes
#76

This is relevant around why lowering glucose levels and peaks can be helpful for longevity:

3 Likes
#77

The size of spike probably matters. I see no evidence that eliminating transient post-prandial increases (say around 140 mg/dL or a bit higher) which go back baseline in 2 hours are harmful especially with a blood profile you noted earlier and the youngish age. Probably better to spend time and effort elsewhere. Also, I haven’t looked at the ITP study, but my guess is that it was not carried out on mice in ideal health. Plus, dosage conversion from mice to humans is an ongoing issue.

1 Like
#78

I agree about Attia and diet. I prefer experts like Walter Willet and Gary Fraser who have studied diets academically for decades and can show a lot of what I consider to be solid evidence supporting a plant-centric diet. Would prefer if more people, including Attia, would just not say anything, or admit their lack of depth knowledge, rather than trying to pass off an opinion as fact. He should know better considering the apparent pains he goes to analyze things. I will only listen to his podcast when he has a real expert on.

3 Likes
#79

Do you think about harmful as the same as being not optimal?

Do you see any evidence in the other direction, ie that going up to around 140 vs say just 130 is optimal?

For instance, do you not see this as relevant:

#80

What would be interesting is to see what the normal glucose pattern is for a teenager or someone in their 20s.

As far as I can see keeping below 140ish is a good idea, but one should not particularly worry about post prandial peaks that go up to 140. My CGM charts from early 2022 were much worse than they are now and I often had glucose meandering around the 10mmol/L mark.

1 Like
#81

@John_Hemming What are your thoughts on glycation as one key parts of aging?

Seems to me that that is (slowly) accumulating problem that we’d want to address?

#82

Glycation varies. If you take the issue of glycation of haemoglobin, some is labile and then the second step is more permanent. I have not studied glycation more generally, but I would think it is driven by average glucose levels and does not necessarily remain if average glucose levels come down.

Hence if you can get your average glucose levels to below pre-diabetic the level of glycation is probably OK. I have not, however, read up on this.

From an aging perspective the damage that high glucose does to mtDNA is probably far more significant than levels of glycation.

2 Likes
#83

Thanks for thoughts @John_Hemming

@Olafurpall any comments on above? I thought it was more difficult to reverse any glycation once it has occurred?

#84

Glycation in proteins that turn over quickly (red blood cells) matters less than long lived proteins. Collagen for example.

AGEs is also in the food you eat. “Browning” of food.

2 Likes
#85

Thanks Joseph.

Is the amount of glucose in our food and blood a part of driving how much glycation there is of such longer lived proteins too?
(Our Blood reaches basically every cell / proteins in the body I think)

1 Like
#86

@Neo Here’s a thread where we took a deep dive into the topic around a podcast I did with two scientists studying this topic. These scientists are focused on the AGEs we eat but the conversation touched on both eaten and formed in body from high glucose.

I don’t recall all the details. What I have taken into my lifestyle is to avoid fried / grilled / dry cooked foods. I also add vinegar to my dinners. I have also added the components of glylo into my stack (b6, b1, ALA, nicotinimide) and with unknown AGEs benefit (but these supplements are useful for life in general).

3 Likes
#87

Yes, there is a distinction between no observed harm and optimal, but is it meaningful in this case? I don’t know. I would have to look back over the available literature if I saw a need to spend time away from other issues to reassess this and still get it wrong or find there is no solid answer - I’m not sure an optimal value (a single number) is known.

You might find the discussions on spikes and CGM data on the Nourished by Science Youtube channel useful, or not. Presented by a PhD in nutrition.

One strategy I employ is to walk after eating. At 70 yo, and WFPB for 12 years, and daily exerciser for same, my HbA1c has stayed at 5%, plus or minus 0.1% for years.

3 Likes
#88

It’s not ok at all even if you have glucose levels below pre-diabetic levels, unless you consider it ok to experience age-related damages, as long as they are at the rate of someone that takes good care of his health. Fact is, glycation is driven primarily by average the glucose concentration and there is no glucose level that is so low that it will result in no glycation occurring. So even if you have a glucose level of under 100 mg/dL you will still experience a lot of glycation. It will just take you a little longer to reach the same level of glycation you had gotten if you had a considerably higher glucose level.

I strongly disagree with that. I think damages it does to the extracellular matrix, resulting in stiffer tissues all over the body, is probably worse than what it does to mtDNA. I notice that you tend to explain almost everything through the lens of mitochondria being the cause and solution to aging. I think they are very important, but just one piece of a much larger puzzle. mtDNA is just one of thousands of types of molecules damaged by glucose in the body. In addition, damage by glucose is only one of several types of damages that damage mtDNA and not necessarily a substantial contributor of the overall mtDNA damage.

The answer to this is a bit complicated. In general, yes, it’s hard to reverse glycation once it has occurred and there are no good interventions that are effective at doing so and are commercially available. The more detailed answer is that glycation is a process usually involving several steps, the first of which is the attachment of the glucose to the amino group of proteins and other compounds. The last step is the formation of various compounds. In some cases these compounds are harmful AGEs (advanced glycated endproducts). The first steps can spontaneously reverse, but once you are far enough to have formed AGEs it’s too late. AGEs are generally irreversible.

Btw on top of my head, I recall that carnosine has been found to be able to reverse the first stages of glycation (the formation of a Shiff base), but I doubt it’s effective enough to have significant effects on glycation after ingestion, unless perhaps one were to take very large doses of it. See this study:

3 Likes
#89

Very helpful @Olafurpall

Besides diet/exercise do you take any medicines to help lower glucose?

Any thoughts on SGLTi’s and especially Canagliflozin in metabolically fit and healthy individuals?

1 Like
#90

I see mtDNA and senescence as being at the centre of the cause of the failure of somatic renewal. The biochemistry of glycation is the same in all species. I dont see it affecting healthspan.