- Messages
- 166
- Type of diabetes
- Type 2
- Treatment type
- Tablets (oral)
The latest article from Prof Roy Taylor is now available on The Lancet site - Link. Reading the full text is free but requires registering an account with The Lancet.
In the paper Taylor has a table listing all the suspected causes of Type 2 that have been suggested in recent years and his counter-arguments. He goes on to explain his research in a way that appears to be intended for doctors to read quickly, the TL;DR version. He also elaborates on something extremely interesting - Taylor might actually have identified a reason why going low-carb is a very fine approach indeed to achieving remission.
From the article:
"The earliest indicator of increased risk of type 2 diabetes is insulin resistance in muscle, a familial characteristic. The everyday practical effect of muscle insulin resistance is the minimal storage of meal-derived carbohydrate as muscle glycogen. In people with muscle insulin resistance, less than 10% of meal carbohydrate is stored in skeletal muscle within 5 h of eating compared with over 30% in people with higher muscle insulin sensitivity. Muscle glycogen concentrations peak around 5 h after a meal and, during a typical day of eating, rise sequentially after each meal. Overnight, concentrations decrease back to the fasting baseline, most likely by exporting lactate to the liver to supply gluconeogenesis. Hence, skeletal muscle acts as a dynamic buffer contributing to the maintenance of plasma glucose within narrow limits. The postprandial storage of glycogen in the liver is determined by the rate of glucose delivery and is similar in people with or without type 2 diabetes and non-diabetic controls.
The glucose not stored in muscle has to be diverted into the alternative pathway of glucose conversion to fat via de novo lipogenesis. De novo lipogenesis produces palmitic acid only, a saturated fatty acid, which is the most potent fatty acid in decreasing β-cell function."
What he's saying here is that the specific saturated fat molecule which the liver produces when it converts carbs into fat is particularly potent at 'switching off' the cells in the pancreas that produce insulin. This fat travels from the liver to the pancreas via VLDL particles (blood triglycerides, basically). My interpretation of this is that eating less carbs might logically result in less of this specific fat type being produced in the body, which might lessen the effect in the pancreas, which might, perhaps, bring about remission a little quicker or maybe even having lost less weight that Taylor suggests is necessary. High blood triglyceride levels might not be such a big problem if the specific fat type contained within the VLDL particles is less harmful to the pancreas.
Do carbs cause diabetes? Well.. actually, that might well be part of it. Maybe. Taylor doesn't say that (at all) but if some fats are worse than others, and excess carbs become the worst kind of fat, it would explain a few things I didn't personally understand about people's varying individual experiences when trying to achieve remission.
Would kindly request that a person read the article that is the subject of this thread, and understand what it says, before commenting.
In the paper Taylor has a table listing all the suspected causes of Type 2 that have been suggested in recent years and his counter-arguments. He goes on to explain his research in a way that appears to be intended for doctors to read quickly, the TL;DR version. He also elaborates on something extremely interesting - Taylor might actually have identified a reason why going low-carb is a very fine approach indeed to achieving remission.
From the article:
"The earliest indicator of increased risk of type 2 diabetes is insulin resistance in muscle, a familial characteristic. The everyday practical effect of muscle insulin resistance is the minimal storage of meal-derived carbohydrate as muscle glycogen. In people with muscle insulin resistance, less than 10% of meal carbohydrate is stored in skeletal muscle within 5 h of eating compared with over 30% in people with higher muscle insulin sensitivity. Muscle glycogen concentrations peak around 5 h after a meal and, during a typical day of eating, rise sequentially after each meal. Overnight, concentrations decrease back to the fasting baseline, most likely by exporting lactate to the liver to supply gluconeogenesis. Hence, skeletal muscle acts as a dynamic buffer contributing to the maintenance of plasma glucose within narrow limits. The postprandial storage of glycogen in the liver is determined by the rate of glucose delivery and is similar in people with or without type 2 diabetes and non-diabetic controls.
The glucose not stored in muscle has to be diverted into the alternative pathway of glucose conversion to fat via de novo lipogenesis. De novo lipogenesis produces palmitic acid only, a saturated fatty acid, which is the most potent fatty acid in decreasing β-cell function."
What he's saying here is that the specific saturated fat molecule which the liver produces when it converts carbs into fat is particularly potent at 'switching off' the cells in the pancreas that produce insulin. This fat travels from the liver to the pancreas via VLDL particles (blood triglycerides, basically). My interpretation of this is that eating less carbs might logically result in less of this specific fat type being produced in the body, which might lessen the effect in the pancreas, which might, perhaps, bring about remission a little quicker or maybe even having lost less weight that Taylor suggests is necessary. High blood triglyceride levels might not be such a big problem if the specific fat type contained within the VLDL particles is less harmful to the pancreas.
Do carbs cause diabetes? Well.. actually, that might well be part of it. Maybe. Taylor doesn't say that (at all) but if some fats are worse than others, and excess carbs become the worst kind of fat, it would explain a few things I didn't personally understand about people's varying individual experiences when trying to achieve remission.
Would kindly request that a person read the article that is the subject of this thread, and understand what it says, before commenting.
