The nature of the onset of T2D

[NewdestinyX]

Hey gang,
I was on a long bike ride over the weekend and I think I had an 'epiphany' about our shared disease and I wanted to run it by the rest of you and compare our reading and notes. For the longest time the majority of the science I've read and what was simple logic (to me) made clear that with or without a genetic component to the onset of T2 - obesity was in this equation - big time. So much so that for the 80% group of us who present at diagnosis overweight or obese - there is the possibility to push the D into total remission. I personally know from message boards 3 such people and 1 in my personal life that have 'reversed' (never cured) their T2 in the sense that they can eat 'any quantity' of carb they want without any major spiking but also, more importantly, a return to fasting levels under 5mmoL by the 1.5 to 2hr mark which became possible ONLY after returning to a normal healthy BMI for their body type -(i.e. lost all the weight they needed to).

But even as I was arduously (and rather annoyingly to some) purporting and supporting with lots of science the idea that obesity is in the 'onset trigger list' for 80% of T2's -- the fact that there were 20% of us who were/are 'skinny T2's' -- close or nearly perfect BMIs (Body Mass Index) STILL taunted at my conclusions above.

Today something hit me - an 'order of events', if you will - an aetiology of the events leading up to the onset of T2.. Now to give vredit where it's due - several very helpful and well informed folks at other forums offered aspects of what I'm about to 'pitch' here -- so this isn't all original in ANY way.. But ------

WHAT IF ----- the 'nature' of the onset of T2 diabetes, IN ALL OF US -- STARTS as a genetically predisposed (or environmentally induced) breakdown in communication between the liver and pancreas that we ALL share in common -- skinny and large alike.. So essentially-THAT'S the 'DISEASE's' NATURE -- a breakdown in communication in pancreatic/liver signalling systems.. From all forms of MODY to LADA to T2 itself (not T1 of course).
Then:
1) - for skinny diabetics - the breakdown is so harsh and rapid from its onset - that extra weight just isn't a complicating issue. The handwriting's on the wall in terms of becoming full blown D. For many of these people exercise and diet change can indeed control BG and possible slow the progression but most in this group will end up on insulin to control. (last statement is both conjecture and from data I've gathered)
2) for the overweight diabetic - VERY early in the process a bad circular problem started. A person can be overweight or even good BMI at this early stage but:
a) the liver/pancreas comm breakdown leads to hyperinsulinemia as the liver can't tell the pancreas to SHUT OFF dumping insulin and people want to eat ALL the time, endlessly hungry, because of this extra insulin in the system. The insulin in the body at this early stage is still pretty efficient so if this next group of folks is sedentary or just not active or have hormonal imbalances with certain other disease or if near/in menopause - then the body's own insulin does it's #2 job of storing the extra carbs as fat (job #1 of insulin is convert glucose to energy in the muscles)
b) the increased fat stored then -- starts to build up around the pancreas and liver making the communication even harder...
c) Then fat storage starts to build up around the belly - again this is all due to hyperinsulinemia (too much insulin STATYING in the bloodstream) which then in turn clogs the muscle receptors and the BG gets trapped in the blood making the pancreas spit out more and more insulin - killing the depleting nearly 60% of the beta cells - leading to full blown T2.
-------end theory-------------

In the above scenario it would explain why both skinny and overweight people can end up as full blown diabetics. And dispel the 'overly simplistic' view that "we ate our way to T2 diabetes". There is the smallest tidbit of truth is such a statement but it's often simplistically charged about us and is uniformed by a bigger picture - not the least of which is the genetic component too. In the above scenario - obesity is a complicating factor to the onset AND a 'symptom' rather than a primary cause.
It could also explain why catching T2 as early as possible can give both the skinny and fuller T2 a better chance at controlling with diet modification only. Since the less insulin required of the pancreas the better. But also couple explain why each person I've known that's 'put their D into remission' were 'obese at dx' AND 'caught it early'. The obesity for this 80% group of folks 'quickly' becomes the cementer of the movement to 'full blown T2' and the removal of which can improve the communication problem between liver and pancreas which I'm coming to believe is the 'smoking gun' in T2.

Thanks for allowing me to pontificate. Use the thesis for target practice, please. I know I learn that way.

 

[Jenfy]

Some interesting thoughts Newdestiny. I'm one of the "Skinny" T2's and whilst I went though a very long period of being hungry all the time, I lost weight, about a stone and a half, before diagnosis, despite seriously over eating and a desperate craving for anything sweet! Several factors seem to have played a role in my contracting T2, I have been told. Genetics, though not parents but possibly aunts ( my dad was 45 when I was born and most of his siblings were older than him and lived a long way off so I'm sketchy about details!), I was a skinny child, not terribly well nourished, I had gestational diabetes and 2 large babies, but back then no one told me this would raise my risk of a later onset (about 30% I believe). My BMI is currently 23 and only once have I been overweight, when I gave up smoking and ate for England! That was many years ago, as were my pregnancies.
If you are right, I was always going to develop diabetes, despite my healthy diet and exercise regime for many years. And also despite this I am having to reduce carbs, exercise more and take meds with little sustained reduction so far in BG.
Anyway, I think obesity is a symptom rather than a cause for some people and whilst I can see that I also think we have some control over what we eat and how much we exercise, so maybe if I had lived a sedentary lifestyle and ate what I wanted all the time, I may have ended up in the 80% of people who are obese and have T2. I honestly don't think there is one size fits all answer, but at the same time we were not designed to sit around eating all day and maybe the higher numbers of Diabetes these days is a consequence of that, such a very different lifestyle than pre TV and video games, processed foods and everything with added sugar.
It's good to get on here and pontificate isn't it? Hopefully someone will come back at me on this, maybe even shoot me down in flames, but with debate comes knowledge. x

 

[Snodger]

obesity is a complicating factor to the onset AND a 'symptom' rather than a primary cause.

I was at a lecture the other day at King's College London, where they are doing some of the most cutting edge work on diabetes. As I understood it, they are thinking along similar lines to you: at least part of the issue with T2 is the breakdown in signalling when the body is full.

 

[Patch]

Very interesting post. My own weight gain (and I assume road to T2) started after a road accident as a child. I was 7 years old, and was on my bike, and got ran over by a van. (I wasn't diagnosed T2 until I was about 20 - but I'm certain I'd had it for years - perhaps from the age of 7!)

I was black (no blue!) with bruises from my neck to my waist, and my lip was split open. Liquid diet ('cos I couldn't open my mouth!) for around 2 weeks.

It was following this accident that the weight piled on. I'd guess that (if your theory is correct) the impact and subsequent torso bruising, is what f*cked up the communication between my liver/pancreas.

So now we know the (possible) cause. What's the (possible) rectification action?

 

[Gappy]

To be honest the original post was too long for me to bother reading (lazy short attention span!) But seeing Patch's post about torso impact rings a bell with me too. In 2006 I had a motorbike accident, spleen, bowel & colon were damaged. Nil by mouth for about 3 weeks due to colon damage so several similarities in the story there.

 

[Sanober]

Hello there

what a very interesting post there! Totally spoke to me on the leeway factor regarding how much can someone who does have means to lose weight and eat differently can influence their T2 diabetes and those who don't have that.

slim, young-ish (34?) and T2, genetics yes - two T2 parents diagnosed in 50s, excessive weight, one on insulin, and one first cousin T2 at 22 (that's it so far) - and also another factor to consider, ethnicity...I'm S.East asian.

So the odds are stacked against me, and I've been told on several occasions by my DN that my diet is overall very healthy and I exercise 3 - 6 hours a week and have been doing so for many years.

Therefore, for me, 'the writing's on the wall'

I quote you here

It could also explain why catching T2 as early as possible can give both the skinny and fuller T2 a better chance at controlling with diet modification only.

I even went on to lose 14 pounds in weight, even though I was at the higher end of normal range to begin with! My BMI's in range also.

My biggest frustration is I've been told I have no leeway as I'm classed as 'optimum lifestyle'.

BUT I've still gone on to make certain change since Dec last year, lowering carbs, avoiding sugar even further, and reducing portion size, I'm normally 1300- 1500 calories a day, these days it's more like 900 -1000... It's been nearly 8mths since my 'pre-diabetes' diagnosis and none of the changes I've made have made much a difference on the glucose numbers, my Hbac1 is still unchanged.

So I do have to accept further assistance from meds eventually, the consultant indicated this would be the case...and I now know he was right.

My insulin production is normal (so I don't have extra insulin floating about...but I used to get the horrible unsatisfied hunger symptom usually after a big and/or carby meal, I remembe crying once!).

My liver's fine. So I think deep down something's broken down more on a cellular level i.e what ever carries the insulin to help the glucose is slowly given up...does the brain influence insulin use? Tying in what you mentioned about the shut off point leading to hunger all the time.

 

[NewdestinyX]

Wow. Thanks everyone who's posted so far. At all forums that I've been at except this one - when you start a thread or post to a thread - the forum interface AUTOMATICALLY adds the thread to your 'subscibed threads' list. This forum doesn't do that. You have to manually subscribe even to a thread you started for it to appear in your list. That's weird and I'd LOST this thread and had to find it again.. And here there are 5 replies.. Sorry.

[I was at a lecture the other day at King's College London, where they are doing some of the most cutting edge work on diabetes. As I understood it, they are thinking along similar lines to you: at least part of the issue with T2 is the breakdown in signalling when the body is full.

Fascinating. I know I'm onto to something here. What they're doing at King's, I'm sure, is more work on Leptin and Ghrelin the stomach hormones.. They are in this equation too but I don't believe they're at the heart of the 'disease itself'. For a disease to be called 'a disease' there has to be some core breakdown in basic and normal function (homeostasis) in the human body. Too often the 'symptoms' of diabetes get center stage and we never attemtp to 'harmonize' the things we have in common in T2. The conclusion becomes an equally simplistic view -- 'we're all just unique' - which I've never believed for a moment - at least not in terms of 'what the disease is and how we got it'. If it's a 'true disease' - we all 'GOT the SYMPTOM of Hyperglycemia' the same way.

For some there were different 'triggers' of the communication breakdown between Pancreas/Liver as Patch and Gabby are pointing out with their accidents. Fascinating. Something may have injured the comm system.

Hello there

what a very interesting post there! Totally spoke to me on the leeway factor regarding how much can someone who does have means to lose weight and eat differently can influence their T2 diabetes and those who don't have that.

Yes. That's the 'exception to the rule' that's been bugging me these last two years. I was VERY fine with accepting that "I ate my way to diabetes" because in terms of my own life story I really hated the way I was becoming but felt powerless to change my eating habits. Getting diabetes T2 was JUST that MIDLIFE project I needed to get healthy again. If it was MY fault -- then I needed to 'DO something about it!'. But still the presence of skinny T2's and the statistic I read - that less than 20% of the world's obese people have or will ever get T2 - haunted me. There has to be a common breakdown - originally - in the organs' proper function, that's either genetic or environmental or both, that 'handpicks its victims', if you will - but MOST importantly is EXACTLY the SAME in all people with the disease. If not - then they should be called different diseases. As T1 is an autoimmune disorder that destroys the pancreas' insulin making ability - there has to be a common aetiology in T2. Science has classified a few other phenomenons and variants of T2 as LADA, and the MODY1-9 series. But I wonder if there is still 'one T2' whose symptom is 'hyperglycemia' eventually.

My liver's fine. So I think deep down something's broken down more on a cellular level

It's not really a cellular breakdown disease from all I've read. But if you have something I could read about that angle please share it!!

i.e what ever carries the insulin to help the glucose is slowly given up

If such a thing were 'broken', as you imply, in the cellular transport system then it wouldn't work 'at all'. Cellular function is either on or off. It's not selective from what i've been taught.

...does the brain influence insulin use?

Not exactly -- the brain's involved indirectly in the sense that when functioning normally a pancreas and liver are doing their jobs 'involuntarily'. So that's the ?? "parasympathetic" nervous system?? I always get that and the 'sympathetic nervous system' mixed up. So point being you 'can't' mentally/voluntarily make the pancreas function a certain way.

Tying in what you mentioned about the shut off point leading to hunger all the time.

That is only so by virtue of there being too much insulin floating around in the blood taking out all the glucose from your bloodstream -which tells the body -- "you're hungry! we need more glucose - please eat!!!". This is also what happens when people use too much basal (Slow acting insulin) to try and get those awesome am numbers. They find they're hungry all day and they go hypo-ish at lunch and dinner. Too much insulin is bad whether from a needle or in your own body. It's a LIFE SAVER for control - don't get me wrong... I couldn't do my life without insulin - but it takes a 'light hand' in its use or it can screw up a lot of things in your attempts to lose weight and stay away from feeling too hungry.

Great input all! More please!!

 

[neilalastair]

Whilst a little OT. I have a good friend who became T1 overnight practically after sustaining a head injury. Since all COMS seems to be dependant on the brain ultimately maybe our shared symptom of obesity and hyergycemia can be found from something being wrong in the brain.
I work in network engineering and when you send a packet of data there is a transmission and an acknowledgement. Perhaps the comm links being down in the liver/pancreas region is just one part of it and there is a bit in the brain.
I know nothing of medicine but throwing random suggestions around the office when networks are broken helps fix stuff surprisingly often.

 

[NewdestinyX]

Whilst a little OT. I have a good friend who became T1 overnight practically after sustaining a head injury. Since all COMS seems to be dependant on the brain ultimately maybe our shared symptom of obesity and hyergycemia can be found from something being wrong in the brain.
I work in network engineering and when you send a packet of data there is a transmission and an acknowledgement. Perhaps the comm links being down in the liver/pancreas region is just one part of it and there is a bit in the brain.
I know nothing of medicine but throwing random suggestions around the office when networks are broken helps fix stuff surprisingly often.

Hmmm. "Fascinating" [as Mr. Spock used to say on the original Star Trek series]