As someone who lived with and almost died from an eating disorder, I have some insight into what might be going through your mind, however, what I will say is a “varied diet”, in my view, needn’t include high amounts of carbohydrate.Because I have a severe eating disorder for 20 years and it’s unlikely I will ever recover but I want to keep trying and hope it will go into remission at some point. Ta important I eat a varied diet from this perspective. I’d rather deal with insulin than an ed
Another battle-scarred ED veteran here. I have not had an active ED for decades, but my relationship with food and nutrition remained pretty much 100% bonkers until metabolic trouble finally led me to low carb. A new understanding of how much better I felt and functioned when fuelled on nutrient-dense, low carb food has been a real eye-opener for me personally. I just wish I had discovered it sooner.As someone who lived with and almost died from an eating disorder, I have some insight into what might be going through your mind, however, what I will say is a “varied diet”, in my view, needn’t include high amounts of carbohydrate.
To me a varied diet means I shouldn’t be living on apples, grapefruit and tomatoes, or just Swiss roll and bacon fries. (Just random examples from my brain.)
I live a reduced carb lifestyle, but do consume carbs - just not lots of them. I have been in a healthy remission for over 10 years now.
Have you discussed the detail of a “varied diet” with your eating disorder folks?
Off topic, I know, and I apologise unresered to @Talya2022 for it, but @andromache , I don’t consider myself battle scarred. Sure as heck I wish it hadn’t happened, but actually both the ED and my treatment taught me a great deal about myself.Another battle-scarred ED veteran here. I have not had an active ED for decades, but my relationship with food and nutrition remained pretty much 100% bonkers until metabolic trouble finally led me to low carb. A new understanding of how much better I felt and functioned when fuelled on nutrient-dense, low carb food has been a real eye-opener for me personally. I just wish I had discovered it sooner.
That kind of statistic, that a Type 2 is likely to need insulin in 10 to 15 years following diagnosis, should be looked at in the context that people tend to put on weight and become less active as they age. There is a still-prevalent assumption amongst the medical community that Type 2 diabetes inevitably progresses, without any solid evidence showing exactly how and why it tends to progress over time.On Semaglutide and blood sugars very well controlled on it. Can’t see me being able to come off it due to not changing to low carb diet. Try to exercise as much as possible. And healthy weight. I’ve read most diabetics will need insulin after 10/15 years. Is this true?
I think you also fail to acknowledge the proportion of T2 who have little to no interest in modifying their eating Gand drinking.That kind of statistic, that a Type 2 is likely to need insulin in 10 to 15 years following diagnosis, should be looked at in the context that people tend to put on weight and become less active as they age. There is a still-prevalent assumption amongst the medical community that Type 2 diabetes inevitably progresses, without any solid evidence showing exactly how and why it tends to progress over time.
The two main issues are insulin resistance and insulin secretion. Roy Taylor proved that weight loss quickly results in the reduction of ectopic fat in the liver, and that this reduces insulin resistance in that tissue in the majority of Type 2 cases. It also either reduces the export of triglyceride from the liver, or if his 'personal fat threshold' theory holds water, it empties out fat stored in adipose (fat cell) tissue which enables more of that tissue to sponge up excess triglyceride from the blood. Lower blood triglyceride levels over time is thought to lead to lower levels of ectopic fat stored in the pancreas. In susceptible individuals pancreatic ectopic fat (droplets of fat inside cells in the pancreas) causes lipid toxicity (fat poisoning) of beta (insulin producing) cells in the pancreas. Reducing pancreatic fat levels leads to at least partial recovery of beta cell function in most recently-diagnosed T2 cases. Taylor suggests that the longer beta cells are exposed to high fat levels the less likely it is that those cells will become fully functional again when lipid toxicity is reduced. He further suggests that a person's genetics determine how resilient their beta cells are and thus how long they can remain in a dysfunctional state and still return to full function, if at all.
You mention that you are at a healthy weight, and if you have lost weight since diagnosis to get there then you've done all you can on the liver and pancreas front. You just need to keep the weight off to keep the fat out of your liver and that side of things is handled. If your weight has remained steady since diagnosis it may be worth investigating Taylor's paper on testing the effects of going from a BMI of around 25 to a BMI of around 22.5. If you're at the mid to lower end of the 'normal' BMI range then there's no solid information available on how to get fat out of your liver - if there's even much in there to begin with.
Aetiology of Type 2 diabetes in people with a ‘normal’ body mass index: testing the personal fat threshold hypothesis
Abstract. Weight loss in overweight or obese individuals with Type 2 diabetes (T2D) can normalize hepatic fat metabolism, decrease fatty acid oversupply to β cells and restore normoglycaemia. One in six people has BMI <27 kg/m2 at diagnosis, and their T2D is assumed to have different aetiology...portlandpress.com
Insulin resistance in adipose and muscle tissue are the other areas that can have a big effect on blood glucose levels. There's no solid information on how to manage insulin resistance in adipose tissue other than, perhaps, weight loss. Insulin resistance in muscle tissue can be improved with regular exercise. Extended exercise will also burn off ectopic fat in muscle tissue, which will cause that tissue to sponge up triglyceride from the blood, which may help to keep levels low and prevent fat build-up in other tissues such as the pancreas. There is a theory that a high blood insulin level is itself the cause of insulin resistance, and if that's true and if it's a reversible condition, a low carb diet may bring down insulin levels and thus lead to lower levels of insulin resistance. I'm dubious of this theory, or if it's true then it might be irreversible, because I have yet to read any reports of people being on low carb diets for years, losing a lot of weight on such a diet, and then finding they can eat a 'normal' amount of carbs again without issue having 'cured' their insulin resistance. There is absolutely no doubt in my mind though that a low carb diet is one that keeps blood glucose levels as low as possible and so is likely to help delay or maybe even prevent the onset of many diabetic complications for a Type 2.
What I'm getting at with all this is that the average Type 2 who might have been expected to need insulin within 10 to 15 years after diagnosis in the past had little to none of this information available to them. They likely put on weight over time and exercised less, and probably ate pretty much the same things they always ate. I'd wager that just by being on this forum your odds might be much better than that old average.
To be fair to him Taylor does pin a lot of the blame on genetics in his book. If his Personal Fat Threshold theory is in fact true, then the root cause of T2 is putting on more weight than an individual's body can handle, with genetics determining the point at which fat starts to accumulate in the liver due to subcutaneous adipose tissue becoming 'full'. He claims that genetics also determines the susceptibility of the liver to insulin resistance due to fat (doesn't happen for the majority of people with fatty livers), and the susceptibility of beta cells to lipid toxicity. He also claims that insulin resistance in muscle tissue has a genetic root.I was reading with great interest - thank you for locating this piece of research - until I got to the bit about "recognising that T2 is due to overnutrition" and then I became - annoyed.
To defend HCPs though, you can only educate a receptive person. Particularly with something like T2 diabetes where so much self management needs to be done. The vast majority of patients are not like those on this forum, who clearly want to learn and self manage and take personal responsibility. Not sure about in other areas but in my area, all newly diagnosed diabetics (T2) are offered an education course. Not sure of the numbers who actually attend. Too many patients tell fibs about what they eat, or nod and smile and go home and return straight to old habits.I think you also fail to acknowledge the proportion of T2 who have little to no interest in modifying their eating Gand drinking.
I am involved in research at our local NIHR, and am repeatedly shocked and disappointed by the number off T2 delegates only interested in the next wonder drug that’ll allow them to carry on as if no diagnosis ever occurred.
Cries of, “ I could never give up bread”, “I do an active job” “I’m just a bad diabetic”, or such like abound, even when neuropathy, strokes or cardiac illness is already in their medical history.
Educarion and timing are critical, and I’m talking of HCPs here.
I don't think Roy Taylor has proved any such thing. He has a theory, which is contradicted by the lived experience of very many people on this forum and elsewhere. Blood glucose control PRECEDES weight loss for us, not follows it. And (in my case at least) at the onset of the condition other diabetic symptoms preceded fat/weight gain - other research indicates that weight gain is effectively another symptom of T2.The two main issues are insulin resistance and insulin secretion. Roy Taylor proved that weight loss quickly results in the reduction of ectopic fat in the liver, and that this reduces insulin resistance in that tissue in the majority of Type 2 cases.
He has proved it, in the majority of cases, conclusively. The numbers are in his papers - lower fasting BG despite lower fasting insulin secretion - the liver is secreting less glucose even though the level of insulin needed to suppress it is less. Lower insulin resistance in the liver. The 12 month postprandial insulin numbers show greatly improved insulin secretion capability over time following fat reduction in the pancreas. Unless something else is going on in all the test cases over those 12 months apart from the initial weight loss, it's the weight loss.I don't think Roy Taylor has proved any such thing. He has a theory, which is contradicted by the lived experience of very many people on this forum and elsewhere. Blood glucose control PRECEDES weight loss for us, not follows it. And (in my case at least) at the onset of the condition other diabetic symptoms preceded fat/weight gain - other research indicates that weight gain is effectively another symptom of T2.
I know a couple of T2s who have not modified their lifestyles or diet and have indeed moved on to needing insulin. Not because they no longer produce their own insulin, but because they need much more than their bodies can produce, given their high carb/low fat diets. As very few of us have had our insulin production measured directly, it's a bit of a leap to assume that all or nearly all T2s aren't producing enough insulin. We clearly can't be at the same time not producing enough insulin, and over-producing insulin so that resistance occurs.
Receptive persons also include HCPs.To defend HCPs though, you can only educate a receptive person. Particularly with something like T2 diabetes where so much self management needs to be done. The vast majority of patients are not like those on this forum, who clearly want to learn and self manage and take personal responsibility. Not sure about in other areas but in my area, all newly diagnosed diabetics (T2) are offered an education course. Not sure of the numbers who actually attend. Too many patients tell fibs about what they eat, or nod and smile and go home and return straight to old habits.
I don't think a 93% failure constitutes success, and that's what their own figures show from the five year DIRECT follow-up. Like many others, you've been taken in by the press releases. I don't think you were a member of these forums when the Taylor material was published, so you may have missed the thread that dealt with this - worth a read.He has proved it, in the majority of cases, conclusively. The numbers are in his papers - lower fasting BG despite lower fasting insulin secretion - the liver is secreting less glucose even though the level of insulin needed to suppress it is less. Lower insulin resistance in the liver. The 12 month postprandial insulin numbers show greatly improved insulin secretion capability over time following fat reduction in the pancreas. Unless something else is going on in all the test cases over those 12 months apart from the initial weight loss, it's the weight loss.
A low carb diet will lower BG levels immediately - no surprise there. I've also read several times on this forum that fasting BG levels are the 'last to fall' on a low carb diet. Last to fall meaning following some weight loss? Or have I misunderstood? How long does it take the average Type 2 adopting a low carb diet to see BG levels drop from a high level to the 'normal' range first thing in the morning?
I don't deny anyone's lived experience or accounts on this forum. I would point out though that even Taylor doesn't claim weight loss works for everyone who has been diagnosed Type 2. Type 2 was defined by exclusion after all - it very probably encompasses a number of similar conditions which are difficult to distinguish and diagnose. This paper (free PDF linked on the page) lists 13 'major' forms of atypical diabetes, many (or most?) of which I believe get diagnosed as generic Type 2. Who knows how many 'minor' forms are known or suspected, or will be identified in future. Taylor being entirely right and contradictory personal experiences are not mutually exclusive.
Atypical Diabetes: What Have We Learned and What Does the Future Hold?
As our understanding of the pathophysiology of diabetes evolves, we increasingly recognize that many patients may have a form of diabetes that does not neadiabetesjournals.org
But you can't blame the HCPs themselves for that, maybe the system we have to work in. Sorry I get massively angry when i read posts moaning about HCPs when behind us is a massive, creaking, inefficient system that let's us all down, patient or HCP. Sure, there are a few bad apples among us but there are in all jobs but we are under enormous pressure day on day with very little time allocated to each patient. If you haven't heard about your course then chase it, chase it, chase it, don't sit back and wait. I can only go by what's on offer in my area. And you've said yourself uptake is low, so why then is that the HCPs fault that no education has been given. Too many people take absolutely no personal responsibility for their own long term conditions, the asthmatic who smokes, the diabetic who eats choc, etc yet expect the NHS to pick them up and sort them.outReceptive persons also include HCPs.
Under The NHS, all newly diagnosed T2s ( certain on T2s, not sure about T1s and others) should be offered an education course within 9 months of diagnosis. 10.5yrs in, I’m still waiting.
Uptake rates for education courses are staggeringly low (averages low single figure percentages, but varies by area), but let’s face it, 9 months in patterns are established and folks have worked out their own ways -successful or otherwise.
To tell someone their condition needs serious attention, then give them a right royal ignoring for 9 months is mixed messaging at best.
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