Around twenty-five years ago in a doctor’s surgery somewhere in the East Midlands:
‘Well Mr Gnome, we have the results of your tests, and I’m sorry to tell you you’re diabetic.’
Even as I asked the stupid question a poorly remembered vision of my grandmother’s leg, adorned with an ulcer as big as my childish hand, flashed across my mind.
‘You’ll need to control your diet, and I’ll give you a prescription for some Metformin and some Gliclazide that will help. You’ll really need to reduce your sugar intake too! I’ll make an appointment with a dietician for you.’
‘Bugger! No more Mars bars!’
So it began.
This article is prompted by our Beloved Leader’s recent blog [I like this “beloved leader” stuff! -Tim] about the ‘invisible diabetics’, the poor souls who are without support and fall below the radar of the NHS. I would hazard a guess that most of those lost souls will be Type Two (T2) diabetics (T2 was formerly known as non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes); unlike the majority of Type Ones (T1) who were, or are, diagnosed in childhood, and are supported, at least to some extent, from the day of diagnosis. There may well be some lost T1s, but they are, thank Gaia (delete and insert whichever deity you prefer), probably few and far between.
Now I appreciate that many of the readers of this blog are pretty knowledgeable about diabetes, and are all reasonably intelligent (some of you terrifyingly so), but the vast majority of you are T1s and may not have an insight into the problems of us T2s. Believe me, it took me a long while to reach the point where I could actually accept that there was a real difference between T1 and T2 diabetes, but in truth, the only real commonality between them is hyperglycaemia.
Diabetes Mellitus, in both its guises, is a failure of the body to process blood glucose into usable energy. (Yes, I know that’s a simplistic definition, but there may be people reading this who aren’t as knowledgeable as the rest of us.) The difference is in the cause; in the case of T1s it’s down to a dysfunctional pancreas; in T2s the causes can be much more complex.
We’ve all heard the cry, ‘If he wasn’t such a fat bastard he wouldn’t be diabetic!’ but did you know that obesity can be one of the symptoms of T2? I just threw that in to point out that you shouldn’t make snap judgements, I also know several T2s who are built like racing snakes.
Having said that though, obesity can play a part in causing T2; in combination with other physiological problems it leads to insulin resistance. Rather than a failure of the body to produce insulin, it’s a failure of the body to use the insulin it produces to process the glucose in the blood.
So, much as it grieves me to admit it, T2s, especially in the early stages of the condition, can’t claim to be members of the Pancreatically Challenged Hordes (or hoards as our Beloved Leader would have it!) [Thanks for pointing out my crappy spelling Terry! -Tim] Thankfully, by the time T2s become insulin dependant, I firmly believe they can claim membership of that august body.
The worst part of T2 diabetes as it affects the general population, is that it can go undiagnosed for long periods, meaning that real physiological damage can already have been caused before any treatment starts. In fact, it’s not uncommon for patients to visit the doctor complaining of the side effects rather than the diabetes; macular degeneration, nephritis, and neuropathy can all be established before other symptoms are recognised.
I would guess the most common symptoms though, are the continual thirst and the need to pee, but being so hyperglycaemic you start falling asleep in your soup can be a symptom, and be pretty funny too! The killer is, that once that damage is done there’s no way to reverse it, and every time your BGL exceeds 13 mmol/L, the damage increases and you start to fry your kidneys. It’s not only the physical problems though; the creeping effects of neuropathy can cause anything from marital stress to severe depression. Sadly, that’s a part of the problem we share with T1s.
By far the best way of treating T2 is to manage the diet and increase the exercise, but that’s not always possible, and for many T2s the pattern from diagnosis onwards is a continual battle to reduce the BG levels. Metformin helps, but one of the side effects of the drug is something similar to irritable bowel syndrome, it’s not pleasant and often the user develops a sensitivity to it that increases the effect to the point the drug has to be discontinued. The next step is insulin dependence.
One of the major differences between T1 and T2 diabetics is the size of the insulin doses required. Whilst a T1 will often measure their dose to the half unit, a T2’s insulin resistance can increase to the point where they are injecting quantities that would have a T1 dead in minutes. Basal doses of Lantus up to ten times that of other SUoPU members, and similar quantities of NovoRapid have been noted on this site alone.
Where T1s walk a knife edge in trying to maintain their balance between hypo and hyper, a T2 struggles continually to pull down their BG to reasonable levels. For a T2 it’s probably a case of managing the doses to provide the maximum utilisation of the insulin with the minimum number of injections.
In the end though, both T1s and T2s share the curse of hyperglycaemia, but T2s don’t run anywhere near as much risk of regular hypoglycaemia that is the bane of the T1. Though we may be at opposite ends of the chart, we are on the same axis; the Brotherhood of the Banjaxed Body gives us a common bond.