Hypoglycaemia is a major factor preventing insulin-treated patients from ac
hieving normoglycaemia. This reflects the inadequacy of current insulin tre
atment, which causes high insulin concentrations in the post-absorptive per
iod. Physiological defences to hypoglycaemia include autonomic activation,
which limits the fall in glucose level and causes symptoms, alerting patien
ts to an impending episode. Many patients develop defective responses and h
ypoglycaemia unawareness after longstanding disease or with tight glycaemic
control and are then prone to severe attacks. This may be the result of re
peated hypoglycaemic episodes, which by altering cerebral glucose uptake, d
isturb the mechanisms that activate the central response to hypoglycaemia.
Preventing further hypoglycaemia can partially reverse these defects and re
store symptomatic awareness. Clinical hypoglycaemia has also been implicate
d in the 'dead in bed' syndrome and in chronic cognitive impairment. The pr
oblem of hypoglycaemia will eventually be solved by better insulin delivery
and non-invasive glucose meters, but until then, more focused education ma
y have a more substantial impact.