What if those childhood symptoms were never “just growing pains”?
The kid who trains 20 hours a week and still can’t keep up with peers who train half as much. The teenager who starts every game strong but fades in the second half — coaches call it “lack of focus.” The straight-A student who is inexplicably exhausted every single morning, napping in every car ride, but nobody worries because the grades are fine.
What if these aren’t personality quirks, laziness, or growing pains? What if they’re the early signs of an energy production problem that won’t be diagnosed for another five years?
1 Five patterns that only make sense in retrospect
After studying the mechanisms of ME/CFS (myalgic encephalomyelitis/chronic fatigue syndrome) for over a year, I’ve identified five clinical patterns that patients and families consistently describe when looking back at the years before diagnosis. Each one, individually, looks completely benign. Together, they paint a picture of a body running on a lower energy budget than everyone assumed.
1.1 1. The overtrained-but-unfit athlete
A child or young adult trains 15–20+ hours per week across multiple sports. Holidays are spent at training camps. The effort is genuine — nobody questions their commitment.
But they never achieve fitness proportional to that effort. Peers with less training are faster, recover more quickly, improve more visibly. The individual is always tired, naps at every opportunity, and gets dismissed as “not trying hard enough.”
The mechanism: a lower ceiling of mitochondrial ATP production. The training load repeatedly hits a metabolic wall that peers never reach. The body can’t produce the energy needed for the supercompensation cycle that makes training work — so the training accumulates stress without producing adaptation. This is not deconditioning. They are training. It’s failed adaptation.
The adult equivalent: the person who exercises religiously for years but never improves, and is inexplicably wrecked after workouts that others find routine.
1.2 2. The late-game fader
A child begins every game performing well — alert, coordinated, competitive. But as the game progresses, concentration dissolves. Mistakes accumulate. Coordination degrades. Parents and coaches call it inattention, lack of motivation, poor competitive spirit.
The mechanism: the brain doesn’t degrade gracefully under energy scarcity. When available ATP drops below a critical threshold, the brain appears to abruptly deprioritise executive function — attention, decision-making, coordination — in favour of basic motor control and survival functions. The cognitive fade is sudden (within minutes), not gradual, and worsens predictably with duration and intensity.
This looks exactly like ADHD inattentive type. But ADHD inattention is constant. This version is triggered by sustained effort and recovers with rest. That distinction matters — and is almost never assessed.
1.3 3. The always-tired high performer
Perhaps the most insidious pattern. A child who performs well at school, does sport, has friends, maintains activities — and appears completely healthy to the outside world.
But they are profoundly tired every single morning. They nap at every opportunity. They have no energy for socialising after structured activities. They function by burning through reserves that others hold in surplus.
Nobody investigates because the metrics look fine. Intelligence, drive, and compensatory strategies mask an energy deficit that only becomes visible when a threshold stressor — a bad infection, a growth spurt, exam season — collapses the fragile equilibrium.
The adult version: the high-achiever who needs 10+ hours of sleep, can’t sustain social life alongside work, and “has no energy for hobbies.”
1.4 4. The shaky hands
A young person with fine hand tremor — “shaky hands like old ladies” — for which no neurological cause is identified. Worse when tired. Fluctuates with activity level. Dismissed as “nervous” or “just how they are.”
The mechanism: fine motor control requires continuous rapid adjustments that consume ATP. When mitochondrial output is marginal, precision degrades into visible tremor. Recent research shows that 53% of children with postural orthostatic tachycardia syndrome (POTS) have small fiber neuropathy on skin biopsy (Moak et al. (Moak et al. 2024)) — degrading the proprioceptive feedback that fine motor control depends on.
1.5 5. The catalogue of “nothing” symptoms
Cold hands and feet — “poor circulation” (Wyller et al. (Wyller et al. 2007) documents abnormal thermoregulation in adolescent ME/CFS). Dizziness on standing — “growing too fast.” Sleep that never refreshes despite adequate hours. Brain fog after sport or exams — “just needs more rest.” Catching every infection that goes around. Craving salt. Crashing on weekends and holidays while appearing fine during the school week.
Each one individually: unremarkable. Collectively: a pattern of autonomic dysfunction and energy insufficiency that is invisible until you know what you’re looking at.
2 The evidence
This isn’t just pattern recognition from patient stories. There’s data:
German insurance claims data (Wirth et al. (Wirth and Scheibenbogen 2026), N=36,332): Children later diagnosed with ME/CFS had significantly elevated rates of fatigue (OR 2.19), pain (OR 1.55), “somatoform disorders” (OR 1.32), and cognitive impairment (OR 2.93) — diagnosed up to five years before the ME/CFS diagnosis. Those “somatoform” codes are particularly telling: they likely represent doctors seeing real symptoms and having no explanation, so they defaulted to “medically unexplained.” The symptoms were real. The explanation came five years later.
ALSPAC birth cohort (Collin et al. (Collin et al. 2018), N=13,978): Children who later developed chronic disabling fatigue had measurably disrupted sleep — shorter duration, later bedtime, more nighttime awakenings — starting 4–7 years before any fatigue diagnosis. Each additional hour of sleep at age 9 cut later fatigue odds by 39%. Measured prospectively. Not recalled after the fact.
Twin study (Kato et al. (Kato et al. 2006), N=19,192): Premorbid perceived stress — measured 25 years before fatigue onset — predicted chronic fatigue with a 5.81-fold risk increase after controlling for shared genetics. This is a true environmental risk factor, not a personality trait.
3 The unifying idea
All these seemingly disconnected symptoms converge on a single concept: reduced metabolic reserve.
The individual is born with — or develops early — a lower ceiling for energy production. They compensate for years through intelligence, persistence, adaptation. But each vignette above represents a moment when demand briefly exceeds that lower ceiling. Too brief to trigger medical investigation. Too persistent to be normal.
The eventual collapse into ME/CFS happens when an immune trigger — an infection, a vaccination reaction, cumulative physiological stress — permanently reduces production capacity below the minimum needed for daily function. The reserves that should buffer this hit have been quietly eroding for years.
4 The important caveats
This applies to about half of cases. Approximately 50% of ME/CFS begins abruptly after an infection with no identifiable prior symptoms (Jason et al. (Jason et al. 2015)). The prodromal pattern described here applies to gradual-onset ME/CFS specifically.
Most tired children don’t have ME/CFS. The diagnostic error rate in pediatric fatigue referrals is approximately 40% (Geraghty & Adeniji (Geraghty and Adeniji 2019)). These patterns are hypothesis-generating, not diagnostic criteria.
We don’t have the prospective proof. No study has measured exercise capacity in children before ME/CFS diagnosis. No longitudinal study tracks overtrained athletes into ME/CFS. The prodromal composite score is proposed but unvalidated. We can recognise these patterns in retrospect — we can’t yet use them to predict who will get sick.
5 Why this matters
Because five years of symptoms dismissed as “growing pains” or “laziness” or “anxiety” is five years of missed opportunity.
Because the child who trains 20 hours a week and keeps getting told to “try harder” may be damaging the very system that’s already failing.
Because understanding that these patterns exist — even without a validated screening tool — means a parent, a coach, a school nurse, a paediatrician might pause before assuming that a tired, underperforming child is simply not trying.
Recognition is the first intervention. And it costs nothing.
Full mechanistic framework: This is part of an ongoing series exploring ME/CFS mechanisms. The book project behind these articles is freely available and updated regularly.