The Hypoglycaemia Guide for T1D, Part 1 of 3
Recognising Hypoglycaemia: Signs, Awareness, and the Nocturnal Picture
A man with twenty years of T1D walks out of a meeting with no idea his glucose is 2.8. The first sign is the wrong word coming out of his mouth. The colleague reaches for the glucose tablets in the desk drawer they have known about for a year. He used to feel his lows. He cannot remember when that stopped.
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Two warning systems, one of them quietens
The body has two layers of warning when glucose drops. The first is the adrenergic response, the body’s alarm system. Sweat, shake, hunger, racing heart, anxious feeling. It tends to start around 3.5 mmol/L (63 mg/dL) and is the warning the early structured-education programmes (DAFNE in the UK, BERTIE, DYNAMIC, GAME) teach families to act on. The second is the neuroglycopenic response, the brain itself running out of its primary fuel. Confusion, slurred speech, vision change, loss of co-ordination, eventually seizure or collapse. It tends to start below 3.0 mmol/L (54 mg/dL).
What happens after years of T1D is that the first system can quieten while the second one stays. The body stops sounding the alarm; the brain still goes hungry. This is not a willpower thing and not a forgetting thing. It is the underlying physiology of repeated lows. The framework comes from the late Philip Cryer at Washington University: hypoglycaemia-associated autonomic failure, or HAAF (Cryer 2013, NEJM). Repeated lows blunt the next adrenaline response, which blunts the next set of symptoms, which leads to lower glucose still. The clinical name is impaired awareness of hypoglycaemia, or IAH. The lived experience is that the first sign of a low becomes confusion or the wrong word in a meeting, not sweat.
Awareness can be measured, and often restored
The clinical name for the loss of warning signs is impaired awareness of hypoglycaemia (IAH), and it is screened in UK adult diabetes clinics with two short questionnaires. The Gold score (Gold 1994, Diabetes Care) is a single question: do you always feel your hypos? A score of four or more, on a one-to-seven scale, signals impaired awareness. The Clarke questionnaire (Clarke 1995) asks eight questions and produces a similar threshold. UK prevalence in adults with T1D, from a Glasgow single-centre study (Geddes 2008, Diabetic Medicine), sits between 19.5 and 25 percent depending on which tool you use, with about a six-fold increase in severe-hypo risk in the impaired-awareness group. The European multi-centre cohort (Pedersen-Bjergaard 2004, Diabetes Metab Res Rev) put the figure higher still: relative risk of severe hypo around 6.2 in the impaired group and 20-fold in the fully-unaware group.
The reversibility piece is the part that does not always come up in clinic. Strict avoidance of glucose below 4.0 mmol/L (72 mg/dL) for three to twelve weeks restores the adrenaline response and the symptoms in many people; the underlying glucagon defect of T1D stays gone (this is permanent), but the warning system above it can come back. The trial evidence is small but consistent: Fanelli 1993 in short-duration T1D, Cranston 1994 in long-duration T1D. The mechanism is the HAAF cycle running in reverse: fewer lows, less blunting, the alarm system rebuilds. The CGM-supported version of this is one of the strongest arguments for setting the low alert at 4.0 mmol/L rather than 3.5; the higher alert catches the lows you would not otherwise feel, and prevents the next blunting cycle.
The nocturnal picture, only visible on the overnight report
Most people who have lived with T1D for a few years can describe the daytime hypo. The nocturnal hypo is the one that often only surfaces when you read the overnight CGM report alongside the diabetes team. The pattern is recognisable once you know it: a slow descent from 11pm to 3am, a flat line below 3.5 mmol/L for forty to ninety minutes, a recovery as the dawn cortisol response kicks in, a wake-up at 5.8 with no memory of anything happening in the night. The body did the work; the brain did not log it.
The two pivotal trials of algorithmic protection against this pattern were both anchored on the overnight pattern specifically. ASPIRE In-Home (Bergenstal 2013, NEJM) tested threshold-based low-glucose suspend in 247 adults and adolescents and showed the area under the nocturnal hypo curve dropped by around 38 percent with HbA1c essentially unchanged. The paediatric extension (Buckingham 2015, Diabetes Care) tested predictive low-glucose suspend in 81 children across 3,420 randomised nights and cut time below 3.9 mmol/L by 50 to 54 percent across both age cohorts, with no increase in morning ketones and zero severe hypo or DKA. These two trials are the algorithmic spine the modern AID systems inherit. The lived consequence is that the overnight CGM report on a current AID system looks materially different from the same person’s report on a non-automated pump from a decade ago.
The overnight CGM report is the conversation, not the spot reading. A nocturnal low you do not feel is still a nocturnal low; the morning HbA1c does not separate it from a flat night. Bring two weeks of overnight reports to the next clinic appointment and ask the team to look at the basal pattern first.
Relative hypo, the high-baseline reader
One pattern that often gets dismissed in clinic is relative hypoglycaemia. A reader who has run high for years, sometimes glucoses above 12 mmol/L (216 mg/dL) for most of the day, can feel hypo symptoms at 5 to 6 mmol/L (90 to 108 mg/dL). The symptoms are real. They are the body’s adrenergic response firing at a glucose level the rest of the population would call normal, because the body has reset its threshold during the high-baseline period. The reader is not making it up; they are reading their own physiology accurately.
The clinical literature describes this as glucose-counter-regulatory threshold shift, and it is part of the same Cryer framework that describes the opposite pattern in long-duration tight-control T1D. The lived consequence is that lowering HbA1c rapidly from a long-standing high tends to feel awful for the first one to three weeks even when the new glucose level is closer to a healthy target. Knowing this in advance changes the conversation: the symptoms are not a sign that the new target is wrong, they are a sign that the body is recalibrating and will. The diabetes team can support a graded reduction over weeks rather than a sudden change, and the CGM-led version of this works particularly well because it lets the family see the symptoms decoupling from the glucose number.
The paediatric framing, ISPAD 2024 Chapter 12
For families with a child living with T1D, the ISPAD 2024 hypoglycaemia chapter (Lange et al, Pediatric Diabetes) is the international anchor. It treats the recognition layer separately for the four age bands the GNL site uses across the platform: infant under 2, preschool 2 to 6, paediatric 7 to 14, adolescent 15 to 17. Below the preschool band, the child cannot tell you they feel low; the recognition piece sits with the parent, the school, the grandparent, the holiday club. The CGM line at 4am becomes the closest thing to a voice the child has, in line with the under-5s rebuild voice that opens this paragraph (the under-2s pattern lives in the Paediatric Lifespan Guide). Above the paediatric band, the young person can feel the lows but is not always willing to say so in front of friends; the recognition piece moves to the conversation about whether glucose alerts are visible to the parent on a CGM share, and how that share evolves through adolescence.
The lived consequence of all of this is that recognition is not a single skill someone learns once. It is a moving target through the years. The under-1 family is reading the cot. The teenager is reading a vibrating watch in maths. The adult who has lived with the condition for two decades is reading a colleague’s face for the look that says you just said something odd. All three are recognition. All three count.
Part 1 of 3
Recognising Hypoglycaemia: Signs, Awareness, and the Nocturnal Picture