Thanks all for the comments, and you are totally correct
@LittleGreyCat - I have kind of left you hanging on the topic of Metformin.
Mainly I forgot, but partly I do feel on less firm ground, because my entire working hypothesis (if you like) is based on a sum total of two weeks of research. I'm not a doctor, I have zero expertise or experience, at least as far as all of this goes. Hell, it took me weeks to figure out that there was a
difference between type-1 and type-2, when I was first diagnosed as a 'definitely diabetic, but not clear which'.
And that's kind of the problem, as I see it; but let me come back to that.
I left the GP on my last visit, armed with my Metformin, and advice that 'it will reduce your insulin resistance'.
That sounded like a good thing, but I couldn't shake the feeling that it was somehow questionable. What was insulin resistance, and by what mechanism could you reduce it (actually the thing that stuck in my mind was the double negative, I had to ask to have it repeated - why would you phrase something so clumsily? - if you 'push something over' - you don't talk about 'reducing its resistance to falling' ... it just seemed like a weird expression, and that was the level I started off thinking- I need to understand this better.
I'm a process engineer by trade - I look at complex manufacturing systems (production lines, typically of high-tech electronic products) and figure out how to make them run better. I look for patterns and I figure out the best knob to turn to make
that dial go
there. It's not about hitting it with a hammer, it's knowing where to hit... That doesn't make me a doctor, but I can't help but look for patterns in the data and I'm always trying to figure out the best way to make the data better.
So - early on I was just engrossed with understanding the way that the insulin doses interacted with the glucose monitor. Being type 2 meant that all of that was totally irrelevant, and that, honestly, annoyed me more than anything.
So - why was the advice on Metformin wrong? well, all caveats about my ignorance aside, Google is your friend, and I quickly lifted this phrase from the National Institute of Health:
In the liver, normal doses of Metformin suppress Glucagon, the hormone responsible for triggering the liver (secreted from the α-cells in the Pancreas) to start gluconeogenesis.
In more simple terms, it prevents the liver producing Glucose (which then goes into the bloodstream) by about 60%.
It's really there as a safety net so that when you have a response to food (deliberately too general - of course it's all about glucose spiking) you don't go hyperglycaemic. Ie, Naturally, your liver produces lots of glucose, and you produce insulin in response, if you can knobble the liver from doing that, you don't get the insulin response, and you don't get the extra glucose in your blood.
Which leads me back to my earlier point - the treatment of Diabetes primarily focusses on reducing the thing that can be measured easily - we have become pretty good at managing HbA1c without really being that troubled that it doesn't statistically make much difference to long term outcomes. Metformin was the best drug to prescribe to reduce blood glucose in the absence of insulin - I don't actually have any issue with that, and all my reading points to it being the best pharmaceutical choice.
However - it's fundamentally trying to solve the wrong problem. Even in that paragraph, the problem is the glucose spike caused by the food (not just too much food, food of the wrong type, eaten in a way that you absorb too much glucose too quickly)
What is insulin resistance? - we all know the answer, instinctively - what is
any resistance? it's just too much of a thing... too much coffee leads to caffeine resistance, too much exercise leads to exercise resistance, and so on... so, any conversation about insulin resistance that doesn't acknowledge that it's just a question of too much insulin must be suspect. You cannot develop insulin resistance without too much insulin any more than you can develop resistance to heroin without ever taking it.
Right? then how do you get too much insulin... you produce insulin when there is too much glucose and fructose too quickly for your liver to cope, and you produce insulin to temporarily store it where it can't do damage - if that happens too often, you develop resistance to insulin, which makes it harder to store away the excess glucose when you need to... and you're into the spiral that ends up with a type-2 diagnosis.
The specific problem for me - was that, with me having done all the above in super quick time by making use of the magical effect of fructose to mess with my liver - I needed to use the best dietary technique to get rid of fat in my liver - which I judge to be the kind of intermittent fasting that goes beyond the liver's store of Glycogen (think temporary quick-release stuff that isn't fat as such, that your liver can use to power your entire body for about 24 hours - it's pretty cool when you realise just what a marvel the liver is...)
Now -
Rewind to what Metformin does - if I'm fasting and then eating an ultra-low carb, zero sugar diet (with more fat than I'm used to, by the way) - what benefit is Metformin to me. None - I just don't have any glucose spikes (which I can see because I'm using a constant glucose monitor). More than that - I can quickly see that my levels have collapsed to nearly normal levels within days of fundamentally changing diet - by any measure I don't need what Metformin offers. (I also don't think I need those Statins, but that's for another time...)
Worse - Metformin will stop the one thing I need to encourage - after my twenty-four hours of fasting and looking forward to another twelve before I can eat (and, Lordy - are those meals fantastic!!) - those extra twelve hours are where my liver is getting a chance to burn off the fat in its reserves, which are full... but how does it do that? - by turning it into Glucose so that the rest of my body can use it in its hard-won state of Ketosis... What does Metformin do again? Stops that very process...
Now - again, none of this is a criticism of my GP or the system in general. What I'm doing has not been agreed with my GP. I could be wrong and doing something stupid (would definitely not be the first time) - I just look for patterns and twist knobs to make the data fit better with my understanding.
So far it seems to be working pretty well. I cannot know whether my liver is recovering, but my understanding of what I'm seeing in my glucose monitor is incredibly encouraging - and nothing is concerning. I don't feel tired, and in fact I feel better on the days I'm fasting - funnily enough, this coincides with the news that our glorious leader does the same once a week, and there has been an explosion in opinions on 36 hour fasting. I can only speak to my experience, which is that I'm losing about a Kg every couple of days, my waist is shrinking, yet I'm eating lots of sausage and bacon, and I feel better than I have in months. My colleague who is type-1 and was on holiday last week commented immediately when he saw me that I looked really well, and that I was looking tired and unwell around Christmas. I take his opinion very seriously.
I would hate for anything I say to be taken as advice and for anyone to harm themselves by doing the same. There are risks - and I'd spent a lot of time thinking this through, testing various scenarios that could present risks, and monitoring myself to make sure my assumptions are correct. 6 months of thinking like a type-1 helps enormously there... please, nobody should take any of this as a suggestion to disregard their GP and stop eating and taking their meds.
I will definitely follow up with more when I talk this through with my GP later this month (can you tell that some of this is rehearsal?) - and if anyone is interested, there is a similar piece on Statins - that's a whole thing to itself... but for now, I've gone and written far too much again....
Best,
Chris
