someone with T2 has actually returned to normal, proper normal.
Are we being guided down a drug dependant road without trying other methods first?
odd day of "normal food"
Have you tried going back to eating around 200g of carbs a day to see if this is true?Once insulin resistance is overcome then your beta cells can function perfectly normally as mine now seem to.
Passing the OGTT without carbing up beforehand?Have you tried going back to eating around 200g of carbs a day to see if this is true?
If not, how do you know your beta cells are functioning perfectly normally? Is there a beta cell function test available?
Not wishing to go down the rabbit hole of conspiracy theories, I will try to answer you a different way. Let us examine those who claim success in apparently slowing down and reversing the inexorable march to insulin dependency and amputation which used to herald a diagnosis of T2D. I am not talking about T1D or those suffering pancreatic insufficiency through disease or surgery. We are in the realms of the Unwins, Taylors, Moseley's who have scientific studies demonstrating some success in making a valid claim it seems. One important point is that what success they achieve seems to be limited - either it only applies to some participants, or it is short-lived and only viable while following their protocols. Return to the land of flowing honey seems still to be beyond our grasp. This site has many success testimonials for dietary interventions, and again, there does not seem to be a diet plan that suits everybody, and again they all need to be maintained for life to prevent relapse.Hello
Today I have another thought. It is just my thought and everyone has their own opinion which i respect and I am in no way disputing or challenging anyone else's view.
I was reading a lot of sites over the weekend (Michael Mosely and David Unwin to name a couple) and there is this thought that it is our B cells going in to a dormant state that causes the resistance to insulin. The cells are not dead or dying but have just gone dormant. It is also possible in theory to wake them up, tap in to additional cells or generate new ones, though I don't think anyone has done that yet.
Why hasn't medical science talked about this? Well there is another theory that big Pharama companies are developing a drug to generate artificial b cells and that the drug industry is so lucrative with so many people depending on drugs that these companies are rubbing their hands together with £ or $ signs in there eyes. Lets face it, if there was a way to not be drug dependant these companies will lose out.
Yes I accept there sadly will be many people who will need to take drugs to control their levels but I believe there will also be a lot of people that could if they wanted to try a more drug free option.
Now my next question is if the human body can fix most other parts or at least to some level, why is it the pancreas that is the exception to the rule? It doesn't make sense to me. Surely there must be instances where eating properly and getting the right "repair ingredients" will crank start my B cells, I would be surprised if there has never been a case where someone with T2 has actually returned to normal, proper normal. There has to be a combination to do this. Diabetes is an epidemic and I don't believe its being treated as say a virus outbreak would be. The general approach seems to be manage it rather than cure it. Correct me if I am wrong here.
I also know for a fact, as I have supported the risk management and medicine management software that huge pharmaceuticals supply GPs with that set "achievements" which are converted in to financial rewards from the government. For example one tick box may be "have 70% of male patients between the ages of 50 and 75 to have a particular screening, or are put on a particular drug". If they achieve this then the GP practice may get £1000 per patient or they could get a lump sum of £25K for example. There are loads of questions, stats, graphs, data mining that the software does. IMHO, pharmas make the drugs by the billions, governments buy them for their health services, GPs need more funding so they prescribe more drugs than is realistically needed, the patient pays for the drugs (unless exempt but then everyone else who pays subsidises these people), the government gets their money back and passes a cut to the GP Practice.
Are we being guided down a drug dependant road without trying other methods first?
Who is to say that instead of being dependant on drugs, there is not another way of managing my Type 2, taking an over all approach that allows for the odd day of "normal food" here and there and generally being strict but with allowances? Maybe a holistic approach rather than eat, measure and react is an option and that it is possible to cut risks and complications and return to a somewhat normal condition by these changes?
Maybe I am alone in this thought, maybe not but its my thought of the day and my hope that one day someone will come up with a cure and not rip off or exploit those who need it.
In this interview, Professor Roy Taylor says that he spend 2 days a week in Clinical Practice (the rest of the time in University research). https://www.bbc.co.uk/programmes/articles/8ZgRfSypm8l8R9ymrTDSg4/q-a-with-professor-roy-taylorProf Taylor is a radiologist - he can take pretty pictures of your inner workings, but he runs the specialist team at Uni, not an HCP practice)
The research by Professor Roy Taylor suggests that if overweight people lose weight soon after diagnosis (about 15 kg for people over 100 kg or 15% of body weight for those under 100kg) they lose fat from the pancreas and beta cells may be 're-awakened' and start functioning again. https://www.ncl.ac.uk/magres/research/diabetes/reversal/#publicinformationThe cells are not dead or dying but have just gone dormant. It is also possible in theory to wake them up, tap in to additional cells or generate new ones, though I don't think anyone has done that yet.
I don't think that this is correct.there is this thought that it is our (assume Beta) B cells going in to a dormant state that causes the resistance to insulin.
According to this, his qualifications are all in physics. His degree, his Ph.D., his professorship are all nonmedical, but his research is linked to medical care through his work at Newcastle ac.In this interview, Professor Roy Taylor says that he spend 2 days a week in Clinical Practice (the rest of the time in University research). https://www.bbc.co.uk/programmes/articles/8ZgRfSypm8l8R9ymrTDSg4/q-a-with-professor-roy-taylor
Um ...According to this, his qualifications are all in physics. His degree, his Ph.D., his professorship are all nonmedical, but his research is linked to medical care through his work at Newcastle ac.
https://www.imperial.ac.uk/people/jr.taylor
Classic chicken and egg situation. There are actually two identified types of IR that occur in mainly T2D. One is mitochondrial IR (muscles and subcutaneous fat), and adipose IR (abdomen and visceral fat). They seem to have different trigger mechanisms and not necessarily one single solution, but that is what most people seem to assume the ND diet provides.I don't think that this is correct.
As far as I know the majority of T2s, at least in the early stages, are in a cycle of over producing insulin to counter ever increasing insulin resistance.
Removing fat from tissues, especially internal organs, can reduce insulin resistance and reduce the demands for insulin.
This is usually, but not always, associated with being overweight.
There are a subset of T2s who have a pancreas which is under producing insulin and often this gets worse over time.
These are often slim T2s.
If the pancreas gives up producing insulin the person falls into the confusing category of starting out as T2 but then becoming effectively T1.
There have been many discussions on this.
There was talk a couple of years back of Beta cells in T1s changing so the immune system didn't attack them.
This is an intriguing proposition because it suggests the potential to reduce or cure T1 if the cells can be both revived and protected.
Coming back to the Beta cells going dormant to cause insulin resistance; I can't see the logic behind this as T1s have dormant (or no) Beta cells and they aren't uniformly insulin resistant.
According to this, his qualifications are all in physics. His degree, his Ph.D., his professorship are all nonmedical, but his research is linked to medical care through his work at Newcastle ac.
https://www.imperial.ac.uk/people/jr.taylor
As I pointed out in a similar thread on the topic of ND and beta cell revival, it is important to take on board that this work allows Prof Taylor to declare possible mechanisms by which the results were recorded. This is a single viewpoint taken at one moment in history. He has not proved those mechanisms, and it is for others to take his work and repeat the experiments and also provide some other independent means as proof that what he is claiming is verifiable. Then it becomes a theory, and no longer just a hypothesis. Until it is verified, it remains = 'The Thoughts of Chairman Roy' and we should not give it too much importance beyond its capability. It becomes another tool in the toolbox, Remember that the ND was originally kicked off as a chemical alternative to bariatric surgery, and it must be noted that the surgery also suffers only partial success and similar failure mechanisms over time.Classic chicken and egg situation. There are actually two identified types of IR that occur in mainly T2D. One is mitochondrial IR (muscles and subcutaneous fat), and adipose IR (abdomen and visceral fat). They seem to have different trigger mechanisms and not necessarily one single solution, but that is what most people seem to assume the ND diet provides.
Roy Taylor by his work has concentrated on primarily adipose IR and he ignores the mitochondrial effects. However, the general weight loss that the diet induces would probably greatly assist that second IR by removing any fat seepage into subcutaneous cells as a serendipitous gain. His work will be of great benefit to the diabetic community and advances our understanding of the condition. But it is just the beginning, a stepping stone. And it only worked for 46% of participants who were rigorously monitored and followed up. The results in a more general slice of the public may not reach even this success rate. We are also seeing a drop-off effect with time after the trial concluded, so there is a mechanism there that needs to be staunched and understood.
Maybe but I am not the only one confused then See the following, which appears to merge both an earlier life with the one from Newcastle ac which has no entries pre 1980.
Maybe but I am not the only one confused then See the following, which appears to merge both an earlier life with the one from Newcastle ac which has no entries pre 1980.
https://www.emedevents.com/speaker-profile/roy-taylor
Edit: it seems the NHS is also confused
https://www.england.nhs.uk/author/roy-taylor/
I also note that your version has him being granted honourary physician status, which is unusual if he had already been qualified as a medic.
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