Yes, I’d also looked at the IVGTT/argenine data but didn’t appreciate the timing issues there. Regarding measured insulin rate, I speculate that a “good” outcome on that would make it likely that the curve integral, had it been measured, would also have been good, tho they are not the same thing.Indeed. It is interesting to note the weight gain in just 12 weeks. As regards remission, Taylor has his own definitopn of remissio that differs from the rest of the world. He ignores prediabetes as being a classification. Also, there was no check on medication use post intervention, and at least some 40% continued to use their diabetic meds. The rest of the world requires remission to be sans medication. and a yearly HbA1c to also be non diabetic.
There is a seperate study he did using IVGTT techniques and an argenine block to measure insulin response. The problem with that study was that he combined two different tests into one continuous session, without a break and this in my opinion skewed the results since it is clear from the graphs that the second test started before the first test had washed out. Also the graphs he published seem to show a Stage #1 insulin response, but the timings on the graph are way out, Phase#1 is triggered by amylase release into the saliva starting to break down the simple starches and sugars before reaching the stomach, so there is a rush of glucose immediately available. This enters the blood stream some 6 minutes after eating starts. It lasts less than 15 minutes. But his first IVGTT measurement seems to be taken at 30 mins which is way past the peak. He is also using IVGTT, so is missing the amylase trigger and any other enzyme activity that may be associated with oral admiistration such as GLUT=4 The other problem seems to be that he uses insulin rate as the measurement parameter when really it should be the area under the curve. I have already commented on his use of a special way of reporting the results where he divides the normal insulin rate by effectively BMI so making it weigh dependant. So it is valid when comparing member within the group, but totally skewed by a weight loss intervention over time. Of course a 15kg weight loss showed improved response - its in the maths.
They are not the same thing. The results reported in the text part use the umol.l/sec/m^2 result, i.e. the rate adjusted for body surface area (BMI) and this is the justification used to make the claim that the response improved due to weight loss and pancreatic fat clearance. Now there may well be benefit from the intervention, but there is a question mark (actually at least 2) that makes the quantitative claim invalid.Yes, I’d also looked at the IVGTT/argenine data but didn’t appreciate the timing issues there. Regarding measured insulin rate, I speculate that a “good” outcome on that would make it likely that the curve integral, had it been measured, would also have been good, tho they are not the same thing.
Could you kindly check the timing of the pancreatic fat dissipation? In Taylor's retrospective in Diabetologia Vol.61, pages 273–283 (2018) he states that Counterpoint "demonstrated that over the 8 week study period the level of fat in the pancreas gradually decreased".They are not the same thing. The results reported in the text part use the umol.l/sec/m^2 result, i.e. the rate adjusted for body surface area (BMI) and this is the justification used to make the claim that the response improved due to weight loss and pancreatic fat clearance. Now there may well be benefit from the intervention, but there is a question mark (actually at least 2) that makes the quantitative claim invalid.
The other thing I find difficult to get my head around is that according to the original study, there are claims that the ectopic fat in the pancreas disappeared in the first week of the diet. Now this type of fat (lipids) is notoriously difficult to shift so again I wonder what they were actually measuring on the MRI.
Since we are talking fat removal, then there should be raised ketones. again, this simple test was omitted, even where the Optifast shake manufacturer explicitly mentions this in their literature, it does not seem to be something that the team was interested in for any of the trials. There was no safety check for DKA and no specific check on whether any participants had low c=peptide at the start. You do not lose 15kg of belly fat without noticing it. especially since there was no intensive exercise involved to burn off the calories.
And although a starvation diet was used, understandably, in order to impose a tight version of lab control over what the participants were eating, it was actually not necessary to achieving the weight loss. (In my own case, at diagnosis, I rejected the ND diet as over-severe and simply cut down on calories on my own terms for four months, lopping off 15kg in the process without the slightest difficulty or discomfort. And I'd advise anyone else to try the same as the first line of attack.)Hepatic fat is mainly trigs which get bundled up into lipids for transport by VLDL and LDL to the blood portal. So it is lipid fat even though it is stored as trigs in the liver. The problematic fat that is ectopic fat is lipids in the wrong place i.e. should have been stored in adipocytes, but got pushed into mitrochondria by mistake. This is the fat that is upsetting the beta cells, so was pumped into the pancreas that does not normally store fat. This is not an easy pool to empty since it is not adipose tissue, and does not respond like adipose tissue. So it will not respond to the normal LDL control mechanism. So this fat may well take the full 8 weeks to shift camp. But it is not hepatic fat. But I am surprised that the hepatic fat emptied so fast - most of us suffer from Liver Dump during the first week of a diet and it often lasts several weeks before the blood glucose levels drop. So the ND diet is indeed starvation diet.
Check out some of the shareholders in Counterweight (the NHS recommended meal replacement) against names of people involved in the Direct trials before claiming they are "impoverished".their impoverished PhD students
The diets used were indeed just standard OTC weight loss diet plans - Optifast 800. Exante, and most recently Cambridge Diet. But these diets have been round for yonks I remember my mum attempting Slimfast way back. But there was no claims made by any of these plans to fix diabetes, except a note that it may affect blood sugars. No Remission.And although a starvation diet was used, understandably, in order to impose a tight version of lab control over what the participants were eating, it was actually not necessary to achieving the weight loss. (In my own case, at diagnosis, I rejected the ND diet as over-severe and simply cut down on calories on my own terms for four months, lopping off 15kg in the process without the slightest difficulty or discomfort. And I'd advise anyone else to try the same as the first line of attack.)
Yes its so strange how the word 'Miracle' rhymes so sweetly with $$$. I see Prof Lean is selling his own diet plan, and its based on Oatmeal: = after all he is in Scotland. He seems to have moved on from ND.Check out some of the shareholders in Counterweight (the NHS recommended meal replacement) against names of people involved in the Direct trials before claiming they are "impoverished".
Well, I agree that label would not fit them all. But having myself supervised very many PhD students and research assistants I am aware of their situation and their struggles in general. Without them, research would be much the sorrier.Check out some of the shareholders in Counterweight (the NHS recommended meal replacement) against names of people involved in the Direct trials before claiming they are "impoverished".
Yes, you have a lot of carbs-reduction slack should you need it. Am I in remission? I suppose so, having held my A1c in the range 39-42 for over 18 months and not an ounce of weight regain. No post-prandial spikes of note and typical fbg of 5.2. BMI of 20-21. I am coded at my surgery as in remission. Note that for someone aged 75 this A1c range is well below pre-diabetic.The diets used were indeed just standard OTC weight loss diet plans - Optifast 800. Exante, and most recently Cambridge Diet. But these diets have been round for yonks I remember my mum attempting Slimfast way back. But there was no claims made by any of these plans to fix diabetes, except a note that it may affect blood sugars. No Remission.
Where ND works where these diet plans are not so effective is in wrapping it up in a 'medical setting'. This forum has many members who have attempted to follow your advice as above, but not achieved the desired result. It is very often a case of Wash Rinse and Repeat. A revolving door. Possible, but even you seem to be looking for a different solution hence this thread. It is not so easy. Have you achieved Remission yourself? I suspect the follow on post diet WOE is not working long term, and this is a problem most of us struggle with . It is also a problem with the ND diet plan Life just ain't perfect.
I cannot do ND myself, because I am TOFI with BMI of 21 and 30 years since DX. So i do not qualify. I have decided that for me I will use a minimum of medication and a suitable diet which I am currently in my eighth year. Yes I miss donuts and pecan slices. But I do have them on occasions and do not get any OMG readings so in a way I am almost in remission. I was in remission 3 years ago when my Consultant and a DSN both declared me officially in remission while I was in hospital and not on meds with a third HbA1c below 46. But I consider myself T2D and willing to continue with my diet plan since the alternatives are too terrible. if I survive till Xmas, I fully intend suspending my WOE and enjoy the full board and lodging of the season. It does not scare me - I did it last year and the year before. I have confidence in my pancreas remaining low fat. And I still have keto to fall back on if I need it.
How does he know if the weight gain lost the remission or if the loss of remission is what caused the gain? I firmly believe I gain weight after and as a result of rising levels.Taylor has told me that he has never encountered a single case of a T2D losing their grip on remission other than by weight regain.
Now that is a very good question. Maybe there are plausible mechanisms for the one case but not (or less so) for the other case. I don’t have the knowledge to judge that one.How does he know if the weight gain lost the remission or if the loss of remission is what caused the gain? I firmly believe I gain weight after and as a result of rising levels.
Well how do I get to meet Professor Taylor then? I've already said earlier in this thread that since my last HbA1c I have lost 6 kgs, yet also lost my remission. I have been diabetic for 11 years and am now at my lightest weight for 19 years.
May I ask how you dealt with the condition in the first few months after diagnosis and with what outcome at the end of that period?Well how do I get to meet Professor Taylor then? I've already said earlier in this thread that since my last HbA1c I have lost 6 kgs, yet also lost my remission. I have been diabetic for 11 years and am now at my lightest weight for 19 years.
He would have no issue with oatmeal, being a staunch believer that carbs are not the root of the problem.Yes its so strange how the word 'Miracle' rhymes so sweetly with $$$. I see Prof Lean is selling his own diet plan, and its based on Oatmeal: = after all he is in Scotland. He seems to have moved on from ND.
I am heavily involved with the NIHR, and as a consequence a couple biomedical research units. They are densely populated by PhD students. The vast majority of those are qualified in one capacity or another. They usually have full-time employment, alongside their studies. That said, I have encountered those just notching up through academia, but they are usually in the "exercise" arena.I agree that my start point is not comparable to the ND position, but it is not my intent to construct any such comparison. I have just the narrow aim of testing whether, from where I stand now, I can up my carbs without detriment. I do already know from previous experimentation that my 3 months on 100g (ending with A1c=42) followed by 3 months on 135g left my A1c virtually unaltered (ending with A1c=40). And I agree that going up to 180g will hardly be radical - but it might allow me some welcome extra latitude. Your 200g is a very good level. I too weigh 64kg.
The matter of the 2-year DiRECT remitters: I may be in error, but my reading of the published data (e.g. in the 2019 paper in Lancet Diabetes and Endocrinology, 7(5), pp. 344-355, and also in other papers) is that at 24 months 53 (36%) of the intervention participants (total 149 at baseline) had remission of diabetes, being a subset of those 68 who had been in remission at 12 months. So I don't see where your 6.8% comes from. I also am not clear about the medication factor within the intervention cohort - there are some ambiguities among the various papers.
I sense that the DiRECT investigators take the view that those T2Ds who are very carb-intolerant, and so really do need to keep their carbs well down, are in that position for any of several reasons, including (a) they never did clear their ectopic fat, or (b) they did, but did so too long after diagnosis, or (c) they have some other or additional metabolic deficiency, or (d) are just inexplicably unlucky. And equally I sense that their view is that those who achieve "real" remission, having become normoglycaemic purely through clearing ectopic fat, have no need whatever to even think about carbs subsequently, never mind reduce them. But whether they are right, I cannot tell.
My dealings were in academia where for a long period full-time research students on grants had little liberty (or the time) to supplement with earnings.I am heavily involved with the NIHR, and as a consequence a couple biomedical research units. They are densely populated by PhD students. The vast majority of those are qualified in one capacity or another. They usually have full-time employment, alongside their studies. That said, I have encountered those just notching up through academia, but they are usually in the "exercise" arena.
Low carb. I was in remission by my HbA1c a year later.May I ask how you dealt with the condition in the first few months after diagnosis and with what outcome at the end of that period?
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