|
Reality Check LIVE! we report ... |
|
Hypoglycaemia The hypoglycaemia session in Mueller Hall was well attended, both by the recently diagnosed, and those who’ve been living with D for many years, in the hope of gaining some new insights into one of the least pleasant effects of D. The session began with a fairly technically detailed overview of hypoglycaemia – “How low is low?” (and why the medical literature can’t even agree on that). Whilst symptoms differ, both between people, and even between incidents, the common symptoms are grouped into two categories; autonomic (such as tremor, palpitations, pallor, numbness etc), and neuroglycopaenic (“lack of glucose in the brain” – such as confusion, altered perception/personality, fatigue, potentially leading, if untreated, to seizure, coma, and death). Whilst it is well known that hypoglycaemia essentially arises from an imbalance between the levels of insulin and glucose in the blood, the session further discussed some of the causes behind these imbalances; such as mistimed meals or insulin doses, insulin “depot” (i.e. subcutaneous injection) vs insulin infusion (i.e. pump therapy) or modification of insulin action (such as latent insulin hypersensitivity which often follows exercise). One of the hazards involved with insulin administration from outside the body, is that the insulin only stops working when there is either no insulin left, or no glucose left in the bloodstream, which can lead to severe hypoglycaemia, with only minimal counterregulation to prevent it – the autonomic release of adrenaline in response to falling BSLs, namely stimulating release of liver glycogen. Conversely, in the non-D response, falling BSLs trigger cessation of insulin secretion, and release of the hormone glucagon (the same as comes in the little orange box) from the pancreas, which also acts on the liver to release glycogen. However, a group of researchers in the mid 90s developed a hypothesis known as “hypoglycaemia-induced autonomic failure” – effectively that even when the body’s BSL is falling, the brain can preferentially take up more glucose than the rest of the body (through the GLUT1 receptor, whereas the rest of the body utilises the GLUT4 receptor). Consequently, the brain is initially less effected by the dropping BSL, allowing normal function (which is good), but preventing the body’s autonomic counterregulatory response (which is bad). It has been found that this situation is worsened in those with good glycaemic control – with the tendency for sitting closer to the threshold. This theory accounts for the severe hypos which often appear very quickly, with little or no warning, as well as the BSL tests which are low, but asymptomatic. Whilst the session was very technically detailed, there were many
real life examples, and discussion in the question time which helped
to clarify many of the points which were discussed, including the
long term effects of mild to moderate hypoglycaemia (there is no
evidence of long term neurological effects), and overnight hypoglycaemia.
Daniel |