Oh please don't do these OGT tests. It's futile and damaging to keep repeating them. Please consider that Professor Taylor is quite simply wrong in some of his assumptions and do remember he used very fat people for his initial experiment, which was just that, an experiment to save some people having to have bariatric surgery. You have never been in that category.
Why won't the NHS tell you the secret to treating diabetes?
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kokhongw
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It is interesting to note Dr Roy Taylors observation... on insulin's effect on liver fat
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3609491/
So the focus for individuals should be on finding a sustainable insulin lite approach, of which calorie reduction is only one of them, matching their lifestyle constraints. Any lifestyle changes that substantially lower insulin load as we have observed over the years on this forum... would be helpful ...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3609491/
So the focus for individuals should be on finding a sustainable insulin lite approach, of which calorie reduction is only one of them, matching their lifestyle constraints. Any lifestyle changes that substantially lower insulin load as we have observed over the years on this forum... would be helpful ...
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Ronancastled
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@Tannith
The PFT & visceral fat theory only holds true for those who were insulin resistant purely because of obesity.
Many of his subjects were non-responders although they lost the required 15kg.
He theorised that their T2 had been too long a duration to recover beta cell function.
It may also have been down to secondary factors such as genetics which he never explored.
Their are many routes to insulin resistance, many of which are still not fully understood.
It would appear however that someone who is morbidly obese with short duration T2 & preferably a low diagnostic level have the greatest chance of reversal through significant weight loss.
I would put myself in this category but we are all different.
The PFT & visceral fat theory only holds true for those who were insulin resistant purely because of obesity.
Many of his subjects were non-responders although they lost the required 15kg.
He theorised that their T2 had been too long a duration to recover beta cell function.
It may also have been down to secondary factors such as genetics which he never explored.
Their are many routes to insulin resistance, many of which are still not fully understood.
It would appear however that someone who is morbidly obese with short duration T2 & preferably a low diagnostic level have the greatest chance of reversal through significant weight loss.
I would put myself in this category but we are all different.
HSSS
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I too have read that a single theory does not explain all type 2. It’s as if type 2 is in fact a number of different types all lumped together under one label.
The loss of significant weight makes a rapid and sustained improvement for some - possibly by any method and for those low carbing with only moderate carb reduction. There are regularly people posting in here of such success. These would fit prof Taylor’s model. For them their diabetes seems visceral fat induced. Others lose weight (sometimes more) and see little significant improvement or much less at least. For these it might be genetics, or carb intolerance, or environmental, or who knows what. There is still much unknown.
The loss of significant weight makes a rapid and sustained improvement for some - possibly by any method and for those low carbing with only moderate carb reduction. There are regularly people posting in here of such success. These would fit prof Taylor’s model. For them their diabetes seems visceral fat induced. Others lose weight (sometimes more) and see little significant improvement or much less at least. For these it might be genetics, or carb intolerance, or environmental, or who knows what. There is still much unknown.
If you read the whole article quoted by @kokhongw you will see that it explains that whilst on a v low cal diet FBG will normalise in about a week it takes 8 weeks for the first and second phase insulin responses to normalise to a level close to that of a normoglycaemic. This is why my FBGs, though now quite good, are not an indication of complete remission, just the beginning of it. I therefore have to continue my diet until the 1st & 2nd phase insulin responses also normalise. At home, without complicated equipment and drugs these can only be measured by an OGT.: " Within 7 days of instituting a substantial negative calorie balance by either dietary intervention or bariatric surgery, fasting plasma glucose levels can normalize. This rapid change relates to a substantial fall in liver fat content and return of normal hepatic insulin sensitivity. Over 8 weeks, first phase and maximal rates of insulin secretion steadily return to normal, and this change is in step with steadily decreasing pancreatic fat content. The difference in time course of these two processes is striking."
kokhongw
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Yes... because he is fixated with the idea that calorie reduction is the ONLY sure way of reducing liver fats... even though he noted that it is the substantial lowering of insulin/glucose (by our inference/interpretation, carbs reduction) that will result in reducing liver fat...
kokhongw
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https://www.diabetes.co.uk/forum/th...treating-diabetes.178134/page-19#post-2357466
In this section he already noted that it is the portal vein hyperinsulinemia that determines how rapidly excess sugars gets converted to fatty acid.
And here he notes that these 3 reduces insulin secretion...
- hypocaloric diet
- physical activity
- thiazolidinedione
[edit]
That omission frames hypocaloric diet as the only viable option and clearly leads to millions missing out on the opportunity to explore the possibility of T2D remission thru adequate carbs reduction.
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If you look up the reference (40) cited in the article , you will find that these comments relate to Type 1 diabetics only. They don't have the same hepatic fat accumulation as we T2s do.
Conclusions/interpretation: In patients with type 1 diabetes, insulin resistance was not associated with increased intrahepatic fat accumulation. In fact, diabetic patients had reduced intrahepatic fat content, which was associated with increased fasting lipid oxidation. The unbalanced hepatic glucagon and insulin concentrations affecting patients with type 1 diabetes may be involved in this abnormality of intrahepatic lipid metabolism.
kokhongw
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Exactly. T1D have difficulty getting fatty liver. Because the insulin concentration in the liver can never be high enough vs T2D.
It means that T1D, even if they inject huge amount of insulin, they do not get fatty liver... systemic/circulatory insulin concentration cannot never reach the same level as the secreted insulin. Amy Berger's blog explains why this is so:-
http://www.tuitnutrition.com/2019/03/insulin-glucagon-pancreas.html
But T2D have insulin resistant liver. And chronic hyperinsulinemia via the portal vein will simply mean that it becomes incredibly difficult for T2D to lose liver fats.
So is it logical to eat food that predictably raise insulin levels in the liver if our objective is to lower liver fats? Is a carb lite approach so ineffective and unsustainable in reducing insulin concentration that it should be casually dismissed and ignored?
" I would plan to track BG post prandial levels (plus recording how many gms of carbs in each meal) at 2 hours post meal "- This is exactly what the OGT does. You do it 2 hours post prandial (ie after consuming calories) (more frequently if you like), and you know exactly how many carbs are in the "meal" as the meal consists of precisely 75gms of carbs. If you used normal meals it would be very difficult to get them exactly the same from one OGT test to the next, so it would be a potentially less accurate measurement of improvement over time.
HSSS
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The difference did you eat meals every single day. And if there are too many carbs for you body to deal each time with you add to the stress your system is under. This educates you what individual real foods do to you.
An OGTT is a test (which also stresses the body hence why many of us say don’t keep doing them so frequently) of your response to glucose solution. How often do you have that for dinner?
I don't understand why anyone would have 75g glucose regularly. If I was going to have 75g of carbs in one go I would have a proper meal and get nutrients from it.
In direct response to the question - if after 40 years the NHS hasn't realised that their terrible advice for diets hasn't reduced obesity and the attendant issues that come with that, what makes you think they will change now. The only way I see them changing their minds is a)proper nutritional training of which hardly anyone in the NHS gets, and b)patients from the ground up showing doctors and in turn doctors providing the relevant research proving that a particular diet (and in this case LCHF/Keto/Time restricted eating) works.
I don't think Prof Taylor has "dismissed" the low carb approach. In this and similar articles he has indeed "ignored" it, but that is simply because he is reporting on his research on low calorie diets, so in this context it would just be irrelevant. It is quite proper for him to leave reporting on low carb diets to those who have researched them, as they are the experts on that. David Attenborough reports on wildlife, and Mary Berry makes cookery programmes. Much as I admire David Attenborough, he would not be my go to person if I wanted to know how to make custard.
oldgreymare
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Apologies, but this is missing the point - by testing after every meal (even if if you only have an approximate idea of the carb load) you can build up a detailed picture of your body's specific response to carbs in different types of meals and how this changes depending on diet, exercise, stress, sleep, time of day, frequency of eating - ALL factors that may influence insulin production on an ongoing basis. Self administered OGT is hardly possible on a daily basis and is extremely artificial - IMHO very little help in learning how to manage your metabolism in real life. Pleased that you feel for you the vcal approach can work - how many more weeks before you need to start to reintroduce more food to try to identify your future set point?
"how many more weeks before you need to start to reintroduce more food to try to identify your future set point?" To find that out, I have to do the OGT's. That's why I do them. That's what they are for. When they come out around the middle to lower range of normoglycaemic, I shall know I have reached my Personal Fat Threshold - the rate above which I should turn T2 again. Then I have to set my calorie intake to ensure I stay below that. I'm hoping that won't be more than 4 more weeks, maybe only 2. It depends how much weight I lose in that time and I prefer to go slowly rather than rush it.
And what if there never was any fat in or around your pancreas? What if the beta cells are simply aging? How will you know? When do you stop? Or do you starve yourself more and more trying to achieve a perhaps unachievable goal?
oldgreymare
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Well good to hear that you won't be starving yourself for more than 4-6 weeks going forward. But sorry, I still don't see the relevance of your self administered OGTs - when is your next HBA1c due? If, like so many on these forums, you wish to find a way to achieve non diabetic metrics purely on diet for the long term, then you will need to develop a long term strategy for eating that provides all energy/nutrients requirements - given the poor dietary advice in the western world since the 1970's it feels odd to think that carbohydrates are NOT essential nutrients, but this is fact. What is your protein/fat strategy for the long term to make your remission goals feasible?
Lamont D
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Hi, I have reactive hypoglycaemia.
And to date I have had six extended oral glucose tolerance tests.
All supervised by trained medical staff.
If something happens to you if you drink 75g of glucose.
Which to a lot of diabetics is really irresponsible.
You don't need to do this.
You would be better off, if you kept a food diary.
This would answer most of the questions you are asking of a glucose test.
If you test before and after eating then one hour, two hours and maybe more, if you need to know your spike or other information.
Heed my warnings, because of my first one I went hypo and I spent fourteen hours in hospital because the doctors would not let me go home because I kept going hypo!
Keep safe.
And to date I have had six extended oral glucose tolerance tests.
All supervised by trained medical staff.
If something happens to you if you drink 75g of glucose.
Which to a lot of diabetics is really irresponsible.
You don't need to do this.
You would be better off, if you kept a food diary.
This would answer most of the questions you are asking of a glucose test.
If you test before and after eating then one hour, two hours and maybe more, if you need to know your spike or other information.
Heed my warnings, because of my first one I went hypo and I spent fourteen hours in hospital because the doctors would not let me go home because I kept going hypo!
Keep safe.
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