T2 or NAFLD? ...or, a funny thing happened on the way to the surgery

[BarbaraG]

I’ve been thinking a lot about the twin cycle hypothesis, and potential implications for particular scenarios. Here are a couple.

Two people reach what Roy Taylor calls their “personal fat threshold”. It doesn’t matter what their actual weight is, or their BMI. Their liver and pancreas are stuffed with fat, and they have T2D. But for the sake of argument, let’s say that they are the same weight and height when this happens. Maybe they are twins.

Person A’s weight then holds steady, or increases only marginally. Person B continue to gain weight, ending up 15kg heavier. Then a few years down they line, they both learn about the steps you need to take to reverse diabetes, they get going, and both lose 15kg. Person B is now back to the weight they were when they were diagnosed - and their diabetes has gone into remission. Person A is 15kg lighter, and their diabetes is also in remission - but if they return to the same weight that person B is now, then their diabetes will return!!

Why? Well, because once your liver and pancreas are stuffed full of fat, they can’t really get any fuller. So person B, who continued to add weight after diagnosis, can’t have added any more fat to their liver and pancreas - or not much, anyway. There just wasn’t room. Hence, when they start to lose weight, liver fat decreases, just as it does for person A. And pancreas fat more slowly.

Its just a thought experiment - what do people think?


And here’s another one, in response to the observation that longer duration of diabetes means remission is less likely. Would it make a difference if you had two people with diabetes of equal long duration, one of whose weight has been relatively steady, whereas the other has lost a significant amount of weight several times, and then regained. Enough to allow their liver to ditch much of its fat for a while (and then regain it), but more importantly, enough to allow the islet cells to get unclogged, at least for a while. Long enough to start waking up again, before the weight rebound clogged them up again. Because if the probability that the beta cells won’t recover the function depends on how long they’ve been submerged in fat, then periods when they are not submerged might allow them to recover, and reset the clock, as it were.

Again, a thought experiment. Worthy of investigation?

 

[Melgar]

With your serum lipid results, I'm really looking forward to hearing what you make of that book...

I've started it. He makes, what could be a very boring subject, an enjoyable read. I will certainly let you know. Thanks for the book recommendation.

 

[Melgar]

Fascinating discussion, and I'll add that book to my list. Sorry, article...
@Melgar - For comparison, my triglyceride levels were 1.5mmol/L at the end of Feb; I would say that with roughly half that, you probably just don't need to look at any other lipid level.. you have almost no visceral fat, period.

I should mention that I'm only a 'convert' to the Malcolm Kendrick view of Cholesterol - I have zero actual medical knowledge; but I would thoroughly recommend reading any of his books - there is a lot of detail on all the data and science behind the connection between diet, cholesterol and heart disease, but any level of poking around will start to make you question some of the things we 'know' - and I would think, should make you far more relaxed about your levels of LDL..

Fundamentally, our thinking today is still an evolution of the interpretation of what doctors first saw under a microscope when they were investigating what was rapidly being described as heart disease - stuff that looked fatty and tested for cholesterol - therefore:

We need to eat less cholesterol, because then there will be less cholesterol in our blood, therefore, less to clog up our arteries and give us heart disease.

This led directly to the guidelines shifting to - eat less fat and more carbs. I mean literally - you can look up the guidelines in 1977 - there is a lot of detail, but fundamentally this led to the idea that we should eat less fat and more carbs.

However, the essential theory is full of holes, and even the original, when written out like I've done, doesn't hold water any more... so a more modern interpretation is now;

We need to eat less saturated fat, because there is a connection between saturated fats and cholesterol, so that we have less cholesterol in the form of 'bad' cholesterol, ie, LDL which can become oxidised, thus finding its way past the endothelium and getting stuck in the artery walls, causing plaque and thus heart disease.

However - all of that is still full of holes...

The most obvious thing is that even way back when, there was significant argument about what the composition of arterial plaque actually is, and how it forms - it's horrendously complicated, and there are whole sections of medical science that just were not understood at the time, but there was definitely a counter argument that all plaques were essentially blood clots, and we should be looking at what was causing the blood clots in the arterial walls in the first place, not focussing on one of the ingredients (which turns out to be virtually identical to LDL but totally different in function, and utterly indistinguishable in the day)

It really makes as much sense as, - most of the composition of arterial plaque seems to be red blood cells, so we should eat less food which has red blood cells in it...

Anyway - the next problem with the dietary approach we all 'know' is that you need much more cholesterol to survive than you can possibly eat, and the liver produces most of it. If you eat less food high in cholesterol, your liver simply produces more.... You simply cannot control your level of cholesterol by just changing diet - (in your case, where you are clearly generally fit and eating well)

The next problem is that - the dietary fats we eat - whether saturated, mono saturated, Omega-3, poly unsaturated - whatever, are all packaged up indiscriminately as triglycerides in the intestine (despite what you might think, your body doesn't really care, the 'tri' refers to three fatty acid chains, and they are made up of any combination at hand) and transported around, dropping off the triglycerides as they go. But these have nothing to do with LDL - LDL, or low density lipids, start off life as very low density lipids, because they are stuffed with triglycerides, and carry them, along with a cholesterol molecule. Critically - all the triglicerides in these VLDLs are saturated, because they are all created by the liver - from carbs.

So - there is not, nor can be - any link between dietary fat and LDL. Diary - maybe, but only because of the level of carbs.. eating more carbs as a way of reducing LDL, though - well, that just cannot help.

Back to the Very low-density Lipid - or transport for Triglyceride - when they have done their job of distributing triglycerides, they are like deflated balloons, with only the cholesterol left - this obviously raises the density and is now known as .... an LDL.

The main distinguishing feature of an LDL is that when you take statins, they go down in number. Otherwise, the amount of LDL in your body is totally a function of your liver, and the amount of LDL receptors in your endothelium - the layer of cells that lines your arteries and veins - and which need cholesterol.

The other main feature of LDLs is that when an endothelial cell expresses an LDL receptor, it then (and only then) enters the cell, drops off its precious cholesterol, and is consumed in the process. There is no mechanism which would explain how an LDL can somehow get past the endothelial layer and 'get stuck' in the arterial wall... just none. It was best described as 'sticking a harpoon in the side of a whale, and then going around to the other side of the whale, and expecting the harpoon to come out' - just cannot happen.

That's just the tip of the iceberg. Get into what the Glycocalyx is, read about the work of Ancel Keyes, before and after he testified to congress, the study that Pfizer nearly published that talked about blood clots, just before they bought the company that developed Atorvastatin, Note that the phraseology around 'bad' cholesterol and 'good' cholesterol (neither of which are really cholesterol, but still emotionally connect to the 'eat less cholesterol' theory) just popped into existence at the same time as statins, which are very good at reducing 'bad' cholesterol... but not really anything else - save making a ton of money..

But, what do I know...

@Chris24Main, and sorry it's along reply, so be warned lol
The Clot Thickens. A great read.
I love Kendrick's delivery, let's get that out of the way first. He manages to bridge the divide between a subject that uses highly technical language with an imaginative pictorial analogy as an aid to our understanding of what is most certainly a complex field - almost impenetrable to the lay person, the likes of people like me.

If Kendrick's polemic, and let's face it, it's a polemic, withstands scrutiny - that LDL is not responsible for the formation of plaques, which in turn are thought, in part, responsible for the development of CVD, then it calls into question the established doctrine around the LDL hypothesis. His book gets to the nitty gritty behind the real reason why we get heart disease and it ain't cholesterol, but a process - that the formation of blood clots, drawing in all kinds of stuff,, some of it nasty in the long term, are the real reason why atherosclerotic plaques form and not LDL's. He gets right into it and he is very persuasive, drawing on the ghosts of past research papers that clearly died in the dark. One thing that jumped out at me too was that type 2 can knock 20 years off your life. I wrote that little beauty down.

To further his own hypothesis, and independently too, the way Lean Mass Hyper Responder phenotypes (LMHR's) process fats have tentatively shown that those of us who have clinically excessive levels of LDL's can maintain those high levels without causing plaque increases. We have David Feldman to thank for that one.

I just want to add some thoughts around why these types of studies can die on the vine. I totally 100% accept that research funding and big pharma are a significant reason behind what gets research money and what doesn't.

It's not only money that drives what research takes place, but to a lesser degree it's the academics themselves. If someone has spent their entire teaching and research career promoting and defending research papers and books, and building their careers on those theories, and let's face it, ideas likely born from their PhD's, back in the day, they are not letting that go without a fight. Furthermore, they would have most certainly aligned themselves with their research supervisor, who in turn, most likely steered their young protogies in a particular direction. These folks are not going to let that career boat sail away without a fight.

To illustrate my point on what gets acknowledged and what gets rejected. I know of academics who will not even get passed the preface of a book if they don't agree or don't like the editorial team, or in fact, who the author chooses to acknowledge in that preface. The book and its theories goes in the can, dismissed and unread.

Leading on from that, young researchers and students, in general, are going to know that if they rock that career boat, it may well end their own careers before they have begun. Academia is not that free thinking happy place where ideas are bounced around like beach balls on a warm sunny day. Certainly not at postgrad/doctorate level and beyond. Nope. So .......

YouTube Oreo experiment
The Oreo guy, Nicholas G Norwitz, has definitely rocked a few boats with his 'Oreo lowers LDL experiment. in LMHRs' He is very brave in my humble opinion. No wonder he peppered his explanation with so many caveats, he needs to. He simultaneously stood by his research and distanced himself at the same time! A bit of word Judo. His Interviewer, Dr. Bret Scher was very kind to him, in my opinion. Saying that, I commend his bravery and his exciting research. My point is, I guess, new and innovative ideas and concepts that challenge established ideas (witness keto diets lower blood sugars) , don't see the light of day, even when no money is involved, but simply careers and big egos. Orio guy chose a radical and news worthy idea - That Oreos lower LDL,s in LMHRs, not raises them, to get his idea past that academic minefield.

Kendrick demonstrated those academic pressures wonderfully.

Asd for me, I have breathed a sigh of relief after reading Kendrickl's book. Bring it on.

Sorry lots of run-on sentences. Too many to edit. I have edited this text. I had Dr Palmer as an Interview, the Dr's name was in fact Dr. Bret Scher.

 

[Outlier]

I particularly liked the clear way he explained how research results could be presented to "support" a desired angle when really they didn't.

 

[Chris24Main]

@Melgar - you seem to have inhaled that book in much the same way I did, and I'm very happy that it's brought you some relief- totally with you on your summary of the underlying hypothesis, and the human elements that seem to keep it suppressed - I did follow through on digging out the Pfizer report that he mentions in passing... it really does exist.

I'm trying to work out how to have a sensible discussion about statins when I next have my GP review, because I got absolutely nowhere in challenging the understanding with her, or my dietician. The resistance to discussing anything that did not align with the 'cholesterol is bad' way of thinking was absolute. There are lots of very simple concepts that would seem to upset the central premise, but in both cases, I got 'well, we don't know why some things happen, but we do know that saturated fat leads to increased heart disease' - and the sort of ... eyes glazing over ... until I stopped speaking.

It's a very difficult thing to do in the 10minutes that we typically get to talk, at least in this country. I want to be positive, but I don't want to be railroaded either...

 

[Melgar]

@Melgar - you seem to have inhaled that book in much the same way I did, and I'm very happy that it's brought you some relief- totally with you on your summary of the underlying hypothesis, and the human elements that seem to keep it suppressed - I did follow through on digging out the Pfizer report that he mentions in passing... it really does exist.

I'm trying to work out how to have a sensible discussion about statins when I next have my GP review, because I got absolutely nowhere in challenging the understanding with her, or my dietician. The resistance to discussing anything that did not align with the 'cholesterol is bad' way of thinking was absolute. There are lots of very simple concepts that would seem to upset the central premise, but in both cases, I got 'well, we don't know why some things happen, but we do know that saturated fat leads to increased heart disease' - and the sort of ... eyes glazing over ... until I stopped speaking.

It's a very difficult thing to do in the 10minutes that we typically get to talk, at least in this country. I want to be positive, but I don't want to be railroaded either...

Years of practise @Chris24Main, read, absorb, summerise, utilize, all needed yesterday, of course. I’ve got a nervous tick even thinking about it. Kendrick’s hypothesis certainly made me think, and ultimately gave me peace of mind from the OMG what the hell factor. But like the whole global question ‘do you believe in god’, you edge your bets. I have increased my carbs (fruit) and reduced my saturated fats( cheese, butter, 35% heavy cream.). Let me add, reduced and increased being just a little on both counts, just to see!

And yes, I too have given up on the diabetic nurse dialogue. Same as you, it’s this mysterious ‘thing’ that we have no business questioning, it just is; The end, thank you and goodbye. In response I to have said the end, thank you and goodbye. We will never get those wasted minutes back. My last Dr said much the same thing, don’t question the holy grail. My new Dr however, is much more dynamic and switched on. He's receptive and not the how dare you type. Ed- I should say I am talking about my T2D diagnosis, I have yet to disclose my alignment with this new rad hypothesis. I positively look forward to see what my Dr thinks.

 

[Chris24Main]

The thing is, it's not really a 'new' theory - it was clearly the losing original theory (among other possible explanations of what was causing an increase in 'heart disease' in the early part of the last century), because the 'eat cholesterol, have cholesterol in your blood, thicken your arteries with cholesterol' is much simpler, and therefore easy to get across - and if there is one thing we like as a species, it's a simple explanation for a complex problem.

But the idea that Arterial plaque may just be an end result of the healing process when you injure the arteries isn't at all new, it just feels like it because it's so contrary to the prevailing 'wisdom'.

I think there is a huge parallel with T2D treatment though - I recall in my very first meeting with anyone discussing my initial high blood glucose levels - and being told that type 2 was when 'your body isn't producing enough insulin, or it isn't working the way it should'.

Now, that is (with my totally enlightened opinion having read, oh, a book, and having done zero hours of medical study) an explanation of insulin resistance that depends on the 'internal starvation' model - ie, it is focussed entirely on the effect of insulin on blood glucose without considering the background level of cellular glucose - in other words it supposes that there is something wrong with the ability of the cells to ingest glucose... not that the cells are simply already full of glucose...

It drives the treatment to focus on drugs to 'overcome' that resistance, rather than thinking about strategies for reducing the underlying levels of 'body' glucose.

The thing that confuses me, is that my GP seemed open to this discussion - I mean she initially told me that the Metformin I'd been prescribed 'was to overcome my insulin resistance' - and when I later told her that this was not what it did, but that the effect of it's primary function in people who were not fasting as I was, (ie to limit the liver's ability to produce glucose) would be to reduce blood glucose and thus give the appearance of overcoming insulin resistance... she considered that and actually said 'yes, I can see how that would make sense' and totally supported my plan, and agreed that there was no need for Metformin.

But - when I challenged the supposed benefits of Statins, and offered that statistically it did nothing for overall mortality and in fact gave slightly worse results - she said 'well, take a look at the benefits to your kidneys; we work with meta-studies and there are more endpoints than just death'.

I'm still a little stuck on that as an opinion... as far as I can tell, there are really only some studies that show you can damage the kidneys of rabbits by feeding them fats that they are totally unable to process, and thus, because statins reduce LDL levels, that should mean otherwise healthy humans should take statins for better Kidney heath. You string out that kind of logic across virtually any other scenario, and ask for a prescription, and you'll be ushered straight out of the doctor's surgery, yet here she was making the case, and getting quite cross that I wasn't going along with it..

It's not hard to imagine how frustrating it must be to spend a lifetime in the medical profession, see the worsening outcomes for the population as a whole regarding T2D and the various ways it eventually kills you, including heart disease, and to be confounded by the total lack of willingness to consider that the underlying advice we live by might not be in our best interest..

 

[Outlier]

Bravo!

I speak as one whose arteries are gin-clear yet am under constant pressure to take statins. I read up on lots of research - including the experiments on rabbits! - and especially the research that wasn't even conducted on women, never mind older women. I make my own conclusions and am also up for investigating any more research that is properly conducted and in the public domain.

 

[Melgar]

When I asked the Dr if I needed to go on Statin's as my LDL was high (and it was likely a lot higher as my resumption of carbs preceded my lipid panel test) , he said no. I took comfort in that 'no' reply. That was when I was totally ignorant of the LMHR triad thing. I wonder if he new all about the LMHR phenotype groups and didn't say anything. Anyways, I really haven't had an in depth discussion around statins with him, as usually my failing eye sight takes precedence, but I have an Ac1 review in a couple of months. I don't bother with the diabetic nurses as they seem lacking in any in depth knowledge of anything to do with T2.and diet They just come out with the same rubbish about low fat diets. They hang onto this low fat docterine. They also cling for dear life on the fact that I am 60 whatever ,therefore I am D2, period. So I have canned them. A waste of my time. I'm sure there must be good ones somewhere in the system, I just haven't met them.

I'm not wearing a CGM at the moment, but despite the none diabetic medication I am on, which in fact forces my pancreas to produce insulin, as it's an - it also carries a warning of hypogylcemia' side effect when using this med, I noticed my blood sugars rising ever so slowly again, even on that medication.

Back to the statins if they are suggested by my Dr, which I doubt he would suggest them, I now feel confident in declining them after reading around this very credible challenge to the LDL hypothesis. Sorry for the gramatical choppyness of my reply.

 

[Melgar]

Sorry for my spelling, sheesh.

 

[jpscloud]

@Melgar - you seem to have inhaled that book in much the same way I did, and I'm very happy that it's brought you some relief- totally with you on your summary of the underlying hypothesis, and the human elements that seem to keep it suppressed - I did follow through on digging out the Pfizer report that he mentions in passing... it really does exist.

I'm trying to work out how to have a sensible discussion about statins when I next have my GP review, because I got absolutely nowhere in challenging the understanding with her, or my dietician. The resistance to discussing anything that did not align with the 'cholesterol is bad' way of thinking was absolute. There are lots of very simple concepts that would seem to upset the central premise, but in both cases, I got 'well, we don't know why some things happen, but we do know that saturated fat leads to increased heart disease' - and the sort of ... eyes glazing over ... until I stopped speaking.

It's a very difficult thing to do in the 10minutes that we typically get to talk, at least in this country. I want to be positive, but I don't want to be railroaded either...

I will undoubtedly be pressured on my next diabetic review to take statins, but I will explain (again) that it is a risk I am willing to take - slightly elevated levels are only to be expected given my slide off the rails over the last few years. I'm hoping to stay firmly on the rails from now on, and get my health into a place where I don't need to be badgered to take statins.

Edit: What I mean is - it's your body, you decide what goes in it. If prolonged discussion is going to irritate the Dr, it may not be worth persuing beyond saying you respect her position but are willing to take the risk for yourself.

 

[HSSS]

One issue with the statin argument with a gp is that my bank provided annual travel insurance asks the question “have you been advised to stake statins” as follow up to my T2 diet controlled status. Now because so many of us are (erroneously in my view) offered them we need to be very careful how they document this discussion. If we are told to and refuse, insurance could be denied in the event of a claim they can make related to any cvd event. However if we are offered and decline less so. If it was merely a discussion about them pros and cons I doubt they’d make that stick.

 

[MrsA2]

It's not hard to imagine how frustrating it must be to spend a lifetime in the medical profession, see the worsening outcomes for the population as a whole regarding T2D and the various ways it eventually kills you, including heart disease, and to be confounded by the total lack of willingness to consider that the underlying advice we live by might not be in our best interest..

Now that deaths from heart disease caused by smoking have greatly reduced, and deaths from cancer reduce due to earlier diagnosis and treatment, and deaths from accidents reduce (bless health and safety) the medical profession does seem to have a desire to reduce deaths even more...but surely humans have a limited span and the aim of reducing or delaying all deaths is futile.

From what I've read the days extra of life span due to things like statins are simply that, a few days which in the scheme of 80+ years is negligible .

It's the concentration on length of life that infuriates me. I'm far better motivated to have a good life, with my digits and limbs and eyesight intact than to live for a few days more limping and blind.

I do wish they'd concentrate on quality and motivation and encouragement than pills, medication and duration.

Just my humble opinion, and a bit of a rant, sorry

 

[Chris24Main]

One issue with the statin argument with a gp is that my bank provided annual travel insurance asks the question “have you been advised to stake statins” as follow up to my T2 diet controlled status. Now because so many of us are (erroneously in my view) offered them we need to be very careful how they document this discussion. If we are told to and refuse, insurance could be denied in the event of a claim they can make related to any cvd event. However if we are offered and decline less so. If it was merely a discussion about them pros and cons I doubt they’d make that stick.

Fascinating perspective, and definitely a danger area for me, as I don't think there is any way that I can currently argue that I've only had a vague discussion about Statins - they are clearly on my regular prescription list, and I'm supposed to be taking them - though on some ill-defined temporary pass on account of it being a bad idea to be taking these meds on an empty stomach.. but this is definitely an angle I need to think through before my next appointment - many thanks for that.

 

[Chris24Main]

Now that deaths from heart disease caused by smoking have greatly reduced, and deaths from cancer reduce due to earlier diagnosis and treatment, and deaths from accidents reduce (bless health and safety) the medical profession does seem to have a desire to reduce deaths even more...but surely humans have a limited span and the aim of reducing or delaying all deaths is futile.

From what I've read the days extra of life span due to things like statins are simply that, a few days which in the scheme of 80+ years is negligible .

It's the concentration on length of life that infuriates me. I'm far better motivated to have a good life, with my digits and limbs and eyesight intact than to live for a few days more limping and blind.

I do wish they'd concentrate on quality and motivation and encouragement than pills, medication and duration.

Just my humble opinion, and a bit of a rant, sorry

Thanks for your input..

Couple of things here - on the quality of life versus length - yes, I totally agree with your underlying view that it's quality that counts - as we come to terms with being in the, let's say, second half of our life... it becomes more and more obvious that health is the thing that really matters, and that we are not the unbreakable beings we thought we were in our youths...

However - I'm more and more coming to the thought that there really isn't any compulsion to think in terms of this being a mutually exclusive choice - either long life or a quality life... you can aspire to both, or at least make decisions that give you the best chance of being healthy for longer in your life, and do some things that will reduce the impact of aging..

I'm currently reading 'Lifespan - why we age and why we don't have to, by Dr David Sinclair' - and that's another emerging science that gives a different perspective to aging, what it is, and some practical simple things that you can do to improve your life outcomes...

The example that most critically comes to mind is- statistically... it's a fall that will do you the most damage. In older people (and all of us will relate this to one relative or another) it's falling and damaging a hip that tends to be the point at which people deteriorate, suddenly everything becomes much harder... so, what can you do?? well, the most obvious thing, is make sure you are doing some form of exercise that maintains your balance and grip strength...

Anyone can do that - and it vastly affects the likelihood that you will catch yourself and not do that kind of damage if & when you trip...

That has nothing to do with the underlying science - which is much harder going, and I don't feel qualified to comment - it's really that this stuck with me - of course being able to hold the banister and catch yourself is a critical life skill ... so doing something to keep your grip strong is not just for the young jocks - its something everyone should do...

But - coming back to the other part of your comments - back to the urge to prescribe Statins... as far as long term mortality rates go.. the point with Statins is that your statistical impact of taking Statins is actually to make things marginally worse if you are a man, and definitely to make things worse if you are a woman.

The key thing is that studies can definitely show that Statins are effective at reducing LDL levels - but you have to remember that this is only a good thing if you buy into some variation of the underlying link between dietary fat, cholesterol (meaning LDL; which is totally is not) in your blood and heart disease in the form of cholesterol furred up plaques (which it is not).

In other words, once you get that this whole logical connection breaks down under scrutiny - for example, if you understand that the thing you can see in plaques which looks very much like LDL, but which is far more likely to be LP(a) which plays a part in blood clots and wasn't even known about back when all this was first mooted - you must acknowledge that a drug which reduces something that is therefore unconnected (LDL) is likely not really having the effect that you might think...

There are plenty other examples, and taken together would suggest that even if Statins are effective at reducing LDL - the overall effect on health will likely be poor or statistically insignificant- and it is... but we don't really seem to care as society.. we only seem to care about the measured LDL levels..

It's almost like the measurement is tailored to prove the effectiveness of the drug... makes you wonder why the term 'bad cholesterol' only entered the lexicon at the same time as Statins...

 

[CottonCutiePies]

Hi Type 1 here for 34 years and still learning. Morning spikes when you get up is known in the diabetes world as the dawn phenomenon. Upon waking your liver kicks out a large proportion of stored glucose to give you the energy needed to get out of bed because when we sleep we don't eat so there's no carbs giving us glucose not that we need it while sleeping. The dawn phenomenon usually subsides after a while because your body is doing daily things so relies on what you put in your mouth to produce glucose. Too much and you Spike especially if you don't produce or take enough insulin. Type 2 produce some at a reduced amount whereas Type 1 don't produce any at all due to the pancreas completely shutting down. This is why Type 2 are often given metformin which is given primarily to make the insulin you produce work more efficiently and thus in some cases reduces body fat that makes you weighty. As I said in the beginning I'm type1 and everytime my insulin dose was put up I'd gain weight some call it the weight hormone. I was put on metformin as a trial for Type 1 to see if it would work in the same way as Type 2 which was to improve my insulin work and to make it last a bit longer than usual. Yes I lost several pounds in weight in a short time and that's because it gave me diarrhea for a month. I toyed with the idea of stopping it because I could function unless I wanted to be a queen sitting on her throne. I did eventually stop taking it due to gaining more weight during lock down and sheilding.

Statins are generally prescribed to help keep cholesterol levels down and over weight diabetics will have some amount of above normal levels of bad cholesterol. Mine were good until I had a heart attack. The cardiologist said low cholesterol and blood pressure is what saved my life.over the years I stopped all my heart meds and on the 11th year I had another heart attack 10 days after my 50th birthday (turning 50 was the worst year healthwise due to finding I had things wrong that I was born with) so once again I was put back on my meds, lesson learnt. I was told the heart attack was the same as the first brought on because of diabetes. There was several years back a furore about GPS handing them out to patients like smarties to people of a certain age to keep cholesterol levels in check, thus in turn it was suggested that people who's diabetes is out of control should have them prescribed to keep their level in tact.
Diabetes has a honeymoon period and after that is over, a lot of curve balls are thrown at you. What works for you 1 day or 1 week will get a curve ball thrown in then what you've been doing goes to pot.

The thing about diabetes is that it doesn't choose unhealthy people over healthy people it randomly happens healthy or not. Children usually get it during hormonal changes and so can it in adults. They're still not convinced that it inherited. In my case it was found during my 1st pregnancy and no other family members had it. It was known as gestational diabetes. After giving birth a several months of eating the chocolate I could while pregnant I had to a glucose tolerance test whereby it was declared I was type1, BUT since no other families had it it could go after future pregnancies. After 4 pregnancies and 3 born babies due to misscarrying the 3rd. I was 100% diagnosed as type1. Many years later my maternal grandmother was diagnosed as type 2 and the following year her son my uncle was also diagnosed as type 2 so the genetics are there because my youngest son was diagnosed as type 1 at 16. My son who had been a little chubby had got stick thin and the reason was diabetes without insulin. Now he maintains his weight with a strict diet and an expensive gym membership.

So another difference between type 1 and 2 is, type 1 no or not enough insulin will lead to weight loss I know this as a fact due to how my son look before diagnosis and myself not looking after my diabetes and not taking the correct amount of insulin during a messy break up and divorce I lost 2 stone in less than 2 weeks.this is because the body has nothing to control glucose therefore not producing enough the body goes into starvation mode and uses fat reserves to be able to function. Type 2 will gain gain weight because the fat reserves getting bigger due to the self produced insulin either not being adequate enough or the body not using it efficiently thus soring more fat cells and the liver producing ketones and ketosis which damages organs.

Sugar spikes. I already mentioned the dawn phenomenon. Other spikes usually come after food usually around 1 to 2 hours after eating an non diabetics deal with that because their insulin usually kicks in when their bodies indicate there's glucose on board so there body produces enough insulin to deal with that almost immediately. With type 1 we give a fast acting insulin usually 15 mins before food this then starts working on the glucose on board and the new glucose we're taking in the form of carbsthis generally has a 2 hour gap where it peaks and when insulin is working with the glucose an by the 2 hour mark leading to 3 hrs it should've descended back to normal provided you've taken enough insulin. In type 2 produced enough. If in type 1 it does descend after 2 hours then our insulin to carb ratio is wrong.

It seems like you're rushing through different courses of action because you want results now. But it doesn't work like that. You have to try something for a while so your body gets used to it before you'll see any benefits before you try something else. Remember what works for A most probably won't work for B and vice versa. Another point to make here is unless your GP no matter how good and understanding they are have specialised in All things diabetes then they only have general knowledge of it thus shouldn't make big decisions without consulting your diabetes team who have specialised in all thing diabetes for years before becoming a specialist in diabetes. I'd rather listen to my diabetes team than my GP who has only a general knowledge. Also there other forms and types of diabetes that have since been discovered after my diagnosis. Work closely with your diabetes team and you'll get better results quicker than trying to fathom it out yourself. You're not alone.

Sorry it turned into an essay but there were several points I felt needed explaining to you.

 

[CottonCutiePies]

Also should've mentioned about reading certain books on the subject, don't get bogged down with what's inside the covers Dr A will say one thing DR B will say something completely different and will C and D. Yet if they all put their studies together they'd probably find a cure.

 

[HSSS]

The dawn phenomenon usually subsides after a while because your body is doing daily things so relies on what you put in your mouth to produce glucose. Too much and you Spike especially if you don't produce or take enough insulin. Type 2 produce some at a reduced amount whereas Type 1 don't produce any at all due to the pancreas completely shutting down.

Actually type 2 typically produce a lot of insulin but don’t utilise it well. Eventually after many years of this their production slows down in some cases. Type 2 is a huge range of diabetes- pretty much anything that doesn’t fit into any other category (and includes a fair few misdiagnosed LADA or 3c’s)

This is why Type 2 are often given metformin which is given primarily to make the insulin you produce work more efficiently and thus in some cases reduces body fat that makes you weighty.

metformin primarily works on reducing the amount of glucose the liver dumps, thereby reducing dawn phenomenon. it therefore reduces blood glucose over the day and looks like it has a small effect on reducing insulin resistance, which it may also do independently of this effect

As I said in the beginning I'm type1 and everytime my insulin dose was put up I'd gain weight some call it the weight hormone. I was put on metformin as a trial for Type 1 to see if it would work in the same way as Type 2 which was to improve my insulin work and to make it last a bit longer than usual. Yes I lost several pounds in weight in a short time and that's because it gave me diarrhea for a month. I toyed with the idea of stopping it because I could function unless I wanted to be a queen sitting on her throne. I did eventually stop taking it due to gaining more weight during lock down and sheilding.

Insulin doesn’t only work as a glucose reactant. It has a secondary function to promote fat storage and hinder fat burning. Hence weight gain if ratios are not perfect. In type 1 that’s about balancing intake and doses and in type 2 about high circulating insulin due to resistance. Both result in weight gain

Diabetes has a honeymoon period and after that is over, a lot of curve balls are thrown at you. What works for you 1 day or 1 week will get a curve ball thrown in then what you've been doing goes to pot.

type 1 does. Type 2 doesn’t have a honeymoon. It’s progressive unless tackled at the root cause level.

The thing about diabetes is that it doesn't choose unhealthy people over healthy people it randomly happens healthy or not.

type 1, not type 2. Type 2 is a condition that involves a collection of less than healthy conditions often known as metabolic syndrome. Eg high glucose, impaired fasting glucose, high blood pressure, increased waist measurements and visceral organ fat, fatty liver etc etc

Children usually get it during hormonal changes and so can it in adults. They're still not convinced that it inherited.

type 1 not type 2. They are different conditions, and the difference make a difference when describing them

In my case it was found during my 1st pregnancy and no other family members had it. It was known as gestational diabetes. After giving birth a several months of eating the chocolate I could while pregnant I had to a glucose tolerance test whereby it was declared I was type1, BUT since no other families had it it could go after future pregnancies. After 4 pregnancies and 3 born babies due to misscarrying the 3rd. I was 100% diagnosed as type1.

a glucose tolerance test cannot determine which type of diabetes. It will identify diabetes not the cause of it or type. Gestational diabetes increases the risk of type 2 not type 1. That’s not to say type 1 cannot be found as a result of pregnancy, but type 1 is an autoimmune control whereas type 2 is metabolic.

Many years later my maternal grandmother was diagnosed as type 2 and the following year her son my uncle was also diagnosed as type 2 so the genetics are there because my youngest son was diagnosed as type 1 at 16.

the genetics are different for type 1 and 2.

Another point to make here is unless your GP no matter how good and understanding they are have specialised in All things diabetes then they only have general knowledge of it thus shouldn't make big decisions without consulting your diabetes team who have specialised in all thing diabetes for years before becoming a specialist in diabetes. I'd rather listen to my diabetes team than my GP who has only a general knowledge. Also there other forms and types of diabetes that have since been discovered after my diagnosis. Work closely with your diabetes team and you'll get better results quicker than trying to fathom it out yourself. You're not alone.

Those diagnosed type 2 rarely see a diabetes team. All they get is a nurse at the surgery who sometimes has little more than a few days extra training

Sorry it turned into an essay but there were several points I felt needed explaining to you.

likewise

 

[Antje77]

I agree with all your points @HSSS , except for this one:

Gestational diabetes increases the risk of type 2 not type 1.

Many adult diagnosed T1's had GD long before getting diagnosed with T1.
Like reactive hypoglycaemia, it can be a precursor to both types of diabetes.

 

[Chris24Main]

Thanks for the interjections @HSSS - saved me the effort...
Wow - I mean; that's really a great counter point to all the things I've been leaning into - @CottonCutiePies, a lot of what you are no doubt trying to pass on in good faith - and I do appreciate the effort to help, and I also appreciate that your length of experience totally trumps mine, but a lot of it is just wrong... and more than that, the continued passing on and acceptance of some of this advice is part of the problem for a lot of people.

The science behind the understanding of the mechanisms driving Diabetes of both types is evolving all the time; when you were first diagnosed, the Glycocalyx hadn't even been discovered, and a big thrust of what I'm trying to deal with is that essentially, since lab insulin was developed, most treatment has devolved into a form of 'get the level of insulin right in order to get the blood glucose right' -

Prior to that - the very best medical advice was that it was so obvious that a severe dietary restriction was the only treatment for diabetes, that there was no point even doing a study to prove it.
Of course, the problem with that was that a small proportion of patients inconveniently just up and died. So, it's just as well that we can learn...

A lot of what you say may be good advice for type 1 - but fundamentally type 2 should be thought of as a hormone imbalance - you simply have more glucose in your body (cells of various types) that your natural mechanisms (insulin) are struggling to pack more in (all talk of resistance and not utilising insulin properly are essentially this, you can't pack a full cell with more glucose) - thus you have too much glucose and insulin in your blood - both of which are terrible for your endothelium, which drives all the long term health issues.

Lots of glucose all the time is very much not something the human species is evolved to deal with, and insulin, like all hormones, is supposed to be a short sharp shock, not a long term thing.

Any attempt to deal with Type 2 Diabetes, or pre-diabetes which doesn't start with trying to drive down your whole body glucose (in the form of stored fat of course) to allow your natural control mechanisms to deal with the situation in a normal fashion ... is just bad medicine in my albeit flawed opinion.

One thing that supports this is that almost all surgical interventions are very successful very quickly. I'm not for a second saying that therefore everyone should have a gastric band; that would be madness for lots of reasons - simply though - if Type 2 diabetes was really a question of something going wrong with 'insulin not working as it should' or that something is breaking down at the endothelial interface ... then there should be a large range in surgical outcomes, but generally speaking, the underlying glucose and insulin levels come back to normal in a day or two after surgery.

It's all really about reducing the amount of times we overwhelm our limited ability to deal with lots of carbs in our diet -

Also - from the perspective of a Type 1 patient, I'm sure it must seem that I'm 'rushing to find instant solutions' - I know, because I know as a type 1 you just cannot think that way - you have to accept and control. However - there are lots of things you can do for yourself as a type 2 - I just decided to bypass the medical advice I had been given, learn what the current best medical understanding was, and decided that I should be able to prove it to my GP within a month - which so far is going exactly as I predicted..

I actually think your son would benefit hugely from a little of this - I've done the hard diet and exercise thing too, and using a bit more metabolic understanding is so much better and a **** sight more fun and enjoyable - your statement on how starvation works is just so wrong on so many levels I don't know where to begin - again, thanks to HSSS for the fact I don't have to.

Please understand - I'm not making fun, it sounds like you've had a tough time. Many people have; but the advice we live by is part of the problem, we eat the wrong things in the wrong way, that has results which we feel bad about, and then get stuck in the diet and exercise loop of shame... meanwhile the Statin industry still makes $billions and we all buy too many ready meals... and eat too much because they don't make you feel full, and so it goes..

Couple of things to add...
The dawn phenomenon ... I do recall being told that there are some things we just don't understand... but it's no 'phenomenon' - it's very simple really.
I fast more or less every other day - so there are lots of mornings where I can be exercising having had nothing to eat for more than 36 hours. There is no dietary glucose in my system and my liver is by then empty of Glycogen - the short term storage version of Glucose.
Quite often, my blood glucose can go from 4.5 or so up to 9 or 10 - when I know for a fact that it's not coming from anything I've eaten...
It isn't a phenomenon, it's totally natural, and if it wasn't - ie, if we somehow really needed a sugary breakfast to get going - the species would have died out many thousands of years ago. It's a response to Cortisol, another hormone, driven by your Circadian Cycle and in fact the absence of a Cortisol raise in the morning is a fairly bad sign of overall poor metabolic (in the wider sense including sleep and mental wellbeing) health.
My Mother had T2D listed on her death certificate - but lower down, below Malignant Cushings syndrome. What this means in a nutshell, is that she was so angry all the time, that she pumped herself full of Cortisol until it killed her.
If your medical team talk to you about 'the dawn phenomenon' - what they are really saying is that their understanding is decades out of date.

It's been said far better than I can, but Type 1 and 2 are very different, and require very different mindsets. There is a significant danger in assuming that anything you 'know' applies to the other type - and I've spent about as much time diagnosed as Type 1 and Type 2.. I don't really know that this gives me a better insight - I do have a colleague who was late onset Type 1 from 20 or so, and has the same 30 year or so experience - he was invaluable to me coming to terms with being diagnosed Type 1, and has continued to be a great help as my diagnosis shifted - but one thing for sure, I've been very clear that all the stuff I've learned recently mainly applies only to Type 2 - with one fairly significant exception...

Even for type 1's - the key goal from the support team is typically to get your time in range up - so you're aiming for a 'steady' level of about 7 mmol/L of blood glucose, because at a population level that's best for reducing the risk of serious hypo events (totally meaningless for type 2 for the most part, though not totally, depending on meds) - but for long term health... that's still a lot of insulin and glucose to have in your blood, and there is very little attempt to reduce short term spikes, which are also not great - in other words, unless you make some effort to live in a way that reduces your need for insulin (which is all the same things for Type 2, lowering carbs means lowering need for insulin..) - your dosage will just keep slowly getting higher and higher, and even though your 'control of your diabetes' will be good, your long term health outlook will not.

Don't get bogged down by what's between the covers?
@CottonCutiePies - are you really saying - read books but don't actually pay attention to them?
No - again, I'm sure you mean this in good faith, and I also used to think that there was a lot of conflicting dietary advice, but seriously, just burying your head in the sand is not the way forward here...

You can very easily find the point in time where the guidelines changed - eat more carbs and less fat. It isn't conspiracy stuff, you can download the congressional report right here; almost all of the low-fat high-processed stuff can be traced back to that - and nearly all the conflicting advice since is an attempt to explain some effect or other in hindsight - the obsession over Omega-3 oils is one good example; when you understand the background to that, and what 'omega-3' really means.. it's all pretty laughable - I mean there was a point in time that the term 'Snake oil' became a negative - prior to that it was a way of selling something that sounded good, but was based on poor science...

If you really understand that most of the 'fat' in your body originates as saturated fat created in the liver from dietary carbs... most of the advice you get about low-fat diets high in polyunsaturated oils.. well, you see it all in a different light. Moderation, sure, but you can stop stressing about all the stuff you are supposed to feel guilty about, and by the way - when you eat fat, you feel full... and you stop eating; it's like magic... Maybe I should refer to that as 'the Leptin phenomenon'... and it might just catch on.

And please don't tell me that Statins reduce cholesterol - if you really think that, you are saying 'I have no idea what cholesterol is'
You need much more cholesterol, every day, than you can possibly eat - just to stay alive. Your liver creates more cholesterol than you eat.
Statins are very effective, but the effect they have is a little more complex, and based on fairly shaky science. Also as a woman, you do understand that a Low LDL level is actually very dangerous don't you - you were told that when you were prescribed statins, weren't you? That Statins are statistically best for men under 40 who have had a heart attack; that was properly explained?

The reason I was inspired to start this thread, is very much that my experience of being treated as type 1 and then realising that my diagnosis had changed, but also that big chunks of what I had been told could not be simultaneously be true - made me seriously question the advice I was being given, and that I better start taking responsibility for learning some basics about metabolism... Where I went from there has just shaken every piece of advice I had taken as gospel all my life - and I feel like I have a better, more cohesive view of the world of diets and eating, and cooking and buying food, than I ever have.

I very much do not feel like - "don't worry about it, if you put everything together it all washes out".... far from it.
However - I definitely suffer from a propensity to go on a bit...