sb4
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For the longest time I have been in a bit of a catch22. If I eat high carbs my heart pounding (my worst symptom) and POTS in general increases significantly yet my gastroparesis doesn't cause much issue. If I eat low carb high fat my post meal POTS / heart pounding is fairly minimal however my gastroparesis flares up significantly.
I have, for the longest time, been trying things to improve my glucose tolerance or improve my gut motility, to make one of these diets work, with only modest success. Methylation/b-vits helped, as did other things but nothing to write home about until now.
For the last 4 days now I have been taking 1/2-1tbsp of MCT oil (C8) with my morning high carb meal. I have been having this meal for a couple of months now every morning and it is around 150g carbs (potatoes) with a little butter and cheese. For the longest time, like clockwork, after eating carbs I experience heart pounding and other pots symptoms starting soon after finishing the meal and climbing until about 1hr postprandial where it reaches its peak, stays there until 1.5/2hrs post and slowly climbs back down to base line over the next couple of hours.
With MCT oil however, I experience heart pounding etc after meal finished up to 1hr increasing, however it is noticeably more mild than before. When it gets to roughly 1hr my heart symptoms decline to near baseline and stay that way. I have only been doing this for 4 days at breakfast only and the result has been the same every day, giving me the confidence to post this thread this early in.
The theory is that something is going wrong with my glucose metabolism. MCTs are oxidized preferentially over glucose. So what I think could be happening is say I have a problem with pyruvate dehydrogenase. When I eat carbs, glucose is delivered to the cell, it goes down the glycolytic pathways to get to PDH where it should be providing the acetyl CoA for TCA to make the energy the cell needs. However, only some gets through so now the cell doesn't have enough energy entering the mito as insulin is suppressing the fat getting to the cell and so it has to make lactic acid to provide the energy. This causes cells / organs / heart to struggle with even basic at rest energy demands and causes the negative symptoms I experience.
With MCTs however, the liver receives glucose and the medium chain triglycerides at the same time. The liver will always give preference to mcts over glucose. So the liver breaks down the 8 carbon fat into a bunch of acetyl CoA. Which then enters the TCA cycle instead of glucose (through PDH). Now the liver has an oversupply of acetyl CoA and a deficit of oxaloacetate, so all the glucose theoretically should go into providing oxaloacetate to allow the TCA cycle to keep spinning. This avoids PDH having to be used.
I am not entirely sure that this is the mechanism at play as I have tried sodium dichloroacetate which should activate PDH without success, as well as PDH cofactors (ALA, Mg, NAD/FAD, Allithiamine) with only mild success.
The video below looks at a study where people ate 300g pasta, 100g tomato sauce with 3tbsps of MCT and they achieved a blood level of beta hydroxybutyrate of 0.3. Mild to moderate ketosis is 0.5-1.5, after a normal glucose meal it is near 0, and normal overnight fast is something like 0.02. So it is providing much more ketones than does overnight fast and is having the oposite effect on ketones as does a glucose based meal.
To enter ketogenesis you most have low oxaloacetate compared to high acetyl CoA. Then the liver sticks 2 acetylcoa together to make ketone bodies that can be used by the brain. Since MCTs can only provide acetyl CoA, this means that once liver glycogen is full, all the ingested carbs alongside MCTs, provided you are making bHB, most be going to oxaloacetate, right? This would completely bypass the need to use PDH.
Here is the video in question. Note that high doses of MCT along with carbohdrate meals are given to epilectic kids, who have to be in ketosis all the time, and it proforms very similar to a keto diet. This could be useful for those of you who have found keto helps @leokitten if you wanted to add more viarety to your diet or just to test if it works.
Any thoughs anyone? @Hip @nanonug @Learner1
I have, for the longest time, been trying things to improve my glucose tolerance or improve my gut motility, to make one of these diets work, with only modest success. Methylation/b-vits helped, as did other things but nothing to write home about until now.
For the last 4 days now I have been taking 1/2-1tbsp of MCT oil (C8) with my morning high carb meal. I have been having this meal for a couple of months now every morning and it is around 150g carbs (potatoes) with a little butter and cheese. For the longest time, like clockwork, after eating carbs I experience heart pounding and other pots symptoms starting soon after finishing the meal and climbing until about 1hr postprandial where it reaches its peak, stays there until 1.5/2hrs post and slowly climbs back down to base line over the next couple of hours.
With MCT oil however, I experience heart pounding etc after meal finished up to 1hr increasing, however it is noticeably more mild than before. When it gets to roughly 1hr my heart symptoms decline to near baseline and stay that way. I have only been doing this for 4 days at breakfast only and the result has been the same every day, giving me the confidence to post this thread this early in.
The theory is that something is going wrong with my glucose metabolism. MCTs are oxidized preferentially over glucose. So what I think could be happening is say I have a problem with pyruvate dehydrogenase. When I eat carbs, glucose is delivered to the cell, it goes down the glycolytic pathways to get to PDH where it should be providing the acetyl CoA for TCA to make the energy the cell needs. However, only some gets through so now the cell doesn't have enough energy entering the mito as insulin is suppressing the fat getting to the cell and so it has to make lactic acid to provide the energy. This causes cells / organs / heart to struggle with even basic at rest energy demands and causes the negative symptoms I experience.
With MCTs however, the liver receives glucose and the medium chain triglycerides at the same time. The liver will always give preference to mcts over glucose. So the liver breaks down the 8 carbon fat into a bunch of acetyl CoA. Which then enters the TCA cycle instead of glucose (through PDH). Now the liver has an oversupply of acetyl CoA and a deficit of oxaloacetate, so all the glucose theoretically should go into providing oxaloacetate to allow the TCA cycle to keep spinning. This avoids PDH having to be used.
I am not entirely sure that this is the mechanism at play as I have tried sodium dichloroacetate which should activate PDH without success, as well as PDH cofactors (ALA, Mg, NAD/FAD, Allithiamine) with only mild success.
The video below looks at a study where people ate 300g pasta, 100g tomato sauce with 3tbsps of MCT and they achieved a blood level of beta hydroxybutyrate of 0.3. Mild to moderate ketosis is 0.5-1.5, after a normal glucose meal it is near 0, and normal overnight fast is something like 0.02. So it is providing much more ketones than does overnight fast and is having the oposite effect on ketones as does a glucose based meal.
To enter ketogenesis you most have low oxaloacetate compared to high acetyl CoA. Then the liver sticks 2 acetylcoa together to make ketone bodies that can be used by the brain. Since MCTs can only provide acetyl CoA, this means that once liver glycogen is full, all the ingested carbs alongside MCTs, provided you are making bHB, most be going to oxaloacetate, right? This would completely bypass the need to use PDH.
Here is the video in question. Note that high doses of MCT along with carbohdrate meals are given to epilectic kids, who have to be in ketosis all the time, and it proforms very similar to a keto diet. This could be useful for those of you who have found keto helps @leokitten if you wanted to add more viarety to your diet or just to test if it works.
Any thoughs anyone? @Hip @nanonug @Learner1