@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.
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There is a different metabolism for glucose over around 8mmol/L (144) that may be part of this.
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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.
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Are you waiting couple hours after meal to measure it?
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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?
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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)
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I actually worked on an aldose reductase inhibitor (ARi) project (one of the key enzymes in the polyol pathway) for over a decade. Great in rodents but it never got beyond early phase clinical trials in humans.
We were working from the rationale that sorbitol accumulation caused osmotic stress to tissues.
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Yes, generally 1 hour post meal but if I get busy as long as it’s within 2 hours I’ll still check it.
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@J0hn That’s interesting. Google says:
" The pathway is implicated in diabetic complications, especially in microvascular damage to the retina, kidney, and nerves. Sorbitol cannot cross cell membranes, and, when it accumulates, it produces osmotic stresses on cells by drawing water into the insulin-independent tissues ."
If I follow…
(1) glucose spikes due to fast absorption of too much glucose for the system to handle (even a healthy person needs some time for insulin to be released or even longer if it needs to be produced because a lot of glucose was consumed)
(2) polyol pathway engaged…among other things, sorbitol is produced from glucose
(3)per the Google blurb: the sorbitol cannot exit the cell…so it accumulates and draws water into the cell. A lot of glucose means a lot of sorbitol, means a lot of water…leads to damage to cell?
True? What happens next…cell has to use the sorbitol for fuel to get rid of it? The ARi would have stopped the production of sorbitol?
That’s right, then sorbitol dehydrogenase converts sorbitol to fructose for metabolism.
It’s been over a decade+ since I worked in the project so my memory is a little hazy but I think there were rate limiting steps in the pathway, that favoured the use of ARi’s.
It was one of the first projects I worked on in 1980, and it had been running for a while before that.
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The best way to treat arteriosclerosis is to prevent it in the first place. Keep your LDL, ApoB, TG and inflammation as low as possible. Take Bempedoic Acid or a statin if you have elevated levels. Eat well and exercise.
That being said, my father is a pescovegetarian and hits the gym several times a week and still has high cholesterol. Sometimes medicine is necessary to avoid tragedy.
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It isn’t more complicated than that. We just need to use safe and effective drugs for us, along with lifestyle changes.
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Believe, it or not it is more complicated than that. While for most people exercising and eating healthy foods it will do the trick, for other does little or nothing. Have a cousin that was near death (survived unfortunately, very disgusting human, the ONLY one that way in all 25 of us) he always was eating only fish with vegies and/or chicken breast with salad. Breakfast oatmeal only. And still he had triple bypass at age 69. Surprisingly, many of us that didn’t watch so much what we ate, do not have any bad blood markers for some reason.
That’s why I said safe and effective drugs to start with.
Is not the 33% figute one step from actual efficacy in humans, which will be subset of the 33%?
Brilliant! Thank you very much
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