The brain is not one organ doing one job. It is a set of regions that each specialise, and that talk to each other all the time through bundles of nerve fibres.
~1.4 kgabout 2 % of an adult's body weight
86 billionneurons, plus about as many support (glial) cells
80 %of all neurons sit in the small cerebellum at the back
What you see in the app
The brain in Brain Energy is drawn midsagittal: cut straight down the middle between the two halves and seen from the inside. This view shows the deep parts (thalamus, hypothalamus, brainstem) that are hidden when you look at the outside of the brain. Front is on the left, back on the right.
The main parts
Part
What it mainly does
Neurons
Cerebrum (cerebral cortex)
The large, folded outer layer: thinking, senses, movement, language, memory. Split into four lobes on each side.
Hearing, language understanding; holds the hippocampus (forming new memories) and amygdala (emotion, threat).
—
· Occipital lobe
Vision.
—
Corpus callosum
The bridge of nerve fibres between the left and right halves. No neuron cell bodies, only their fibres (axons).
~200 million axons
Thalamus
A relay hub: most sensory signals pass through it on their way to the cortex.
~100 million
Hypothalamus
Keeps the body in balance: hunger, thirst, temperature, sleep, hormones. It also senses blood sugar .
tens of millions
Brainstem
Runs life support: breathing, heart rate, blood pressure, waking and sleeping. Connects the brain to the spinal cord.
—
Cerebellum
Coordination, balance and timing; fine-tunes movements and helps learn skills.
~69 billion
Ventricles
Connected spaces filled with cerebrospinal fluid that cushions the brain. No neurons.
0
"—" = no single reliable count. The Regions tab gives each region's count, its source and how sure it is.
Regions work as teams
Most abilities need several regions at once. Remembering a face uses vision (occipital), recognition (temporal), memory (hippocampus) and emotion (amygdala). In the app these teams are called systems (limbic, motor, visual, default mode), and the Functions list shows which regions take part in each function.
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Try it: open the Regions view, click a region to read about it, double-click to split it into its parts, or pick a system on the left.
Basics
Neurons & synapses
Neurons are the brain's signalling cells. Each one collects signals from others, decides whether to fire, and passes its own signal on through thousands of tiny contact points called synapses.
A simplified neuron. Real neurons have many more branches.
The parts of a neuron
Dendrites — branching inputs that receive signals from other neurons.
Cell body (soma) — holds the nucleus and adds up the incoming signals.
Axon — a single output cable, sometimes very long, that splits into many branches. Many axons are wrapped in myelin, a fatty insulation that makes signals travel much faster.
Axon terminals — the branch endings, filled with small bubbles (vesicles) of neurotransmitter.
How a signal is passed on
Firing. When enough input arrives, the neuron fires an action potential: a brief electrical pulse made by sodium ions rushing in, then potassium ions flowing out.
Down the axon. The pulse runs along the axon and into every branch.
At the synapse. The pulse makes vesicles release neurotransmitter (for example glutamate) into a tiny gap, the synaptic cleft.
Next neuron. The neurotransmitter binds receptors on the next neuron's dendrite and nudges it towards firing (or away from it, for inhibitory synapses).
Reset. Pumps push the ions back and the neurotransmitter is cleared and recycled. This clean-up is what costs most of the energy (see Energy Demands).
~150 trillionsynapses in the human neocortex alone
thousandsof synapses on a typical cortical neuron
1 : 1neurons to glial cells in the whole brain
The support cells (glia)
Astrocytes look after the space around synapses, take up glucose from the blood and pass fuel (lactate) to neurons . Oligodendrocytes make myelin. Microglia are the brain's immune cells and clean up damage.
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Try it: open the Neurons view and press Start signals to watch impulses run down axons and across synapses. Zoom in and click a neuron to see everything it connects to.
Basics
Neuroplasticity
The brain's wiring is not fixed. Connections get stronger, weaker, new ones form and unused ones are removed — this is how we learn and remember, and how the brain can partly recover after injury.
"Cells that fire together, wire together"
In 1949 Donald Hebb proposed that when one neuron repeatedly helps to fire another, the connection between them grows stronger . The popular summary is "cells that fire together, wire together".
Four kinds of change
Stronger or weaker synapses
Repeated use makes a synapse respond more strongly for hours to weeks (long-term potentiation, LTP, first shown in 1973) ; little use weakens it (long-term depression, LTD).
New and lost connections
Small dendrite bumps called spines, where most excitatory synapses sit, appear and disappear with experience .
Faster cables
Practice can change myelin, tuning how fast signals travel along axons .
New neurons?
Whether adults keep making new neurons in the hippocampus is still debated: some studies find almost none , others find it continues into old age .
Learning costs energy
Building and keeping connections uses energy. In fruit flies, forming long-term memory shortens survival when food is cut off , and starving flies switch off costly long-term memory to save energy . The brain's budget per neuron is roughly fixed , so plasticity has to fit inside it.
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Try it: in the Neurons view press + Neuroplasticity: each neuron grows a new axon branch towards a neighbour, which grows a dendrite to meet it, and a synapse forms.
Energy
The brain's energy demands
For its size the brain is the most expensive organ in the body. It runs non-stop, day and night, and it has almost no fuel stored.
2 % → 20 %2 % of body weight uses about 20 % of the body's energy and oxygen at rest
~20 Wroughly the power of a dim light bulb (20 % of a resting body's ~100 W)
~10 sto lose consciousness when blood flow to the brain stops
What it runs on
Normally the brain burns glucose (blood sugar) with oxygen, both delivered by blood . It stores very little — a small amount of glycogen in astrocytes — so it depends on a steady supply. During long fasting the liver makes ketone bodies, which can supply most of the brain's fuel . The body protects the brain's supply before other organs, sometimes called the "selfish brain" .
Where the energy goes
Most of it pays for signalling. Every action potential and every synaptic signal lets ions leak across the membrane, and pumps (above all the sodium–potassium pump) must spend ATP to push them back. In grey matter the biggest costs are action potentials and synaptic transmission; keeping neurons at rest and housekeeping cost less .
Housekeeping (making proteins and lipids, moving cargo)
smaller
Exact shares differ between studies and species .
Not every region is equal
Regions differ in how much energy they use and in how well they cope when supply drops. In hypoglycemia, for example, the brainstem and cerebellum are spared while parts of the cortex and the hippocampus are damaged .
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Try it: the Energy view slows the regions the research says lose out first when energy runs short. Press Start and move the energy-deficiency slider.
Energy Deficiency
Causes of energy deficiency
The brain can run short of energy in three ways: fuel arrives but cells cannot use it well, too little fuel or oxygen arrives, or demand suddenly outgrows supply.
A sudden drop or a long, low supply
Sudden drop (acute)
Fuel falls within minutes to hours — a hypoglycemia episode, a night without sleep, a climb to altitude. The brain notices quickly: alarm signals, hunger and stress hormones push supply back up, and thinking and mood change until it recovers. Usually fully reversible.
Chronic low energy
Supply or use is a little too low for months or years — insulin resistance, ageing, poor sleep, failing mitochondria. There is no alarm; the brain adapts by doing less, and the cost shows slowly as weaker memory and thinking and a higher risk of disease.
Critical events — stroke, cardiac arrest, suffocation — cut supply almost completely; they are a third type, outside the focus of this site.
Fuel arrives but cannot be used well
Insulin resistance
Insulin helps memory circuits refuel. In rats, blocking the insulin-driven glucose transporter GLUT4 in the hippocampus stopped the extra glucose uptake that comes with learning, and memory suffered.
The brain itself can become insulin resistant. Post-mortem hippocampus from people with Alzheimer's responded much less to insulin than tissue from people without dementia, even without diabetes, and the blocked signalling tracked worse memory.
Insulin resistance goes with lower brain glucose use. In cognitively normal adults with prediabetes or early type 2 diabetes, higher insulin resistance (HOMA-IR) went with lower glucose use in frontal, parietal and cingulate cortex — the regions hit early in Alzheimer's. The same held in 150 mostly non-diabetic adults around 60, with worse memory.
Diabetes lowers brain energy use without more amyloid. In about 750 older adults, diabetes and HbA1c of 6.5 % or more went with lower glucose use in Alzheimer-type regions, but not with more amyloid.
Treating it: mixed.Mixed A 4-month pilot of nasal insulin improved memory and kept brain glucose use from falling. The larger 12-month trial (289 people) found no benefit, though its delivery device changed midway.
Not that simple.Contrary During an insulin infusion, brain glucose use rose in people with impaired glucose tolerance but not in people with normal tolerance — so "insulin-resistant body, starved brain" is too simple. Brain insulin resistance still has no agreed definition or direct measure in living people, and cause and effect are unproven.
Impaired mitochondria
Mitochondria make most of the brain's ATP from glucose and oxygen. Inherited mitochondrial disease affects about 1 in 4,300 adults and often involves the brain.
Energy-hungry neurons are hit first. A single human dopamine neuron has over 4 m of axon and more than a million synapses, costing far more ATP to signal than a rat's; these neurons have little margin.
Parkinson's. Complex I, the first enzyme of the energy chain, is selectively reduced in the substantia nigra, and its neurons carry high levels of mitochondrial DNA deletions (43 % of copies in the elderly, 52 % in Parkinson's).
Alzheimer's. Cytochrome oxidase (complex IV, the last step of the chain) is less active; one hypothesis puts mitochondrial decline at the start of late-onset Alzheimer's — not yet proven.
Oxidative damage. 4-HNE, a product of fat oxidation, quickly blocks a key Krebs-cycle enzyme (α-ketoglutarate dehydrogenase) and mitochondrial respiration.
Cause or consequence?Limits High-dose coenzyme Q10 did not slow early Parkinson's in 600 people. Whether mitochondrial failure causes the disease or follows from it is still open.
Aldehydes from oxidised fats (4-HNE)
Oxidised fat makes a sticky aldehyde. When the polyunsaturated fats in a membrane oxidise, they release 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA), which attach to nearby proteins and disable them.
It cripples the glucose transporter. In cultured neurons, amyloid-β set off lipid peroxidation; 4-HNE attached to GLUT3, the neuron's glucose transporter, glucose uptake and ATP fell before any neuron died, and 4-HNE alone did the same. Antioxidants prevented all of it. In isolated synapses the same happened within an hour, with the mitochondria making more reactive oxygen and less ATP.
It also stops the sodium pump. 4-HNE lowers the activity of the sodium-potassium pump, the single biggest user of a neuron's energy, and lets calcium leak in.
It also blocks the burning. 4-HNE inhibits two enzymes that burn glucose in the mitochondria (α-ketoglutarate dehydrogenase and pyruvate dehydrogenase), so even glucose that gets in yields less energy. Limits In Alzheimer's brain tissue the picture is less tidy: the enzyme that regenerates their cofactor was lower, but the cofactor was not more HNE-modified.
It is there in the diseases. 4-HNE is higher in Alzheimer's brains, above all in the amygdala, hippocampus and parahippocampal gyrus, and it coats the surviving dopamine neurons of the substantia nigra in Parkinson's disease.
Other transporters, less evidence.Limits 4-HNE causes insulin resistance in muscle within hours, through the signalling step that moves GLUT4 to the cell surface, and in people more 4-HNE in muscle goes with worse insulin sensitivity (correlation only). The astrocyte and blood-brain-barrier transporter GLUT1 is a plausible target. But direct brain studies of 4-HNE on GLUT1 and GLUT4 are lacking; GLUT3 is the proven one. MDA forms similar adducts but has not been studied on the transporters.
Where amyloid-β fits. In Alzheimer's, amyloid-β is one of the ways the peroxidation starts, which makes amyloid a cause of poor glucose use as well as a synaptic toxin. What it does at the synapse is covered in the Neuro-toxicities project.
Vitamin B1 (thiamine) deficiency
Thiamine is needed to burn glucose. The vitamin itself is inactive: cells first convert it to thiamine diphosphate (TPP), which is the helper for three glucose-burning enzymes (pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, transketolase). Without it glucose burning falls, lactate builds up and neurons die in the thalamus, mammillary bodies, brainstem and cerebellum.
More common than diagnosed. Wernicke's brain lesions were found in 1.7 % of autopsies, but only 14 % of these had been diagnosed in life; only 16 % of proven cases showed the classic three signs.
Who is at risk. Alcohol misuse, malnutrition, and weight-loss surgery: after surgery, 94 % of cases appeared within 6 months, 90 % after frequent vomiting, and half did not fully recover.
Alzheimer's. The thiamine-dependent enzymes are less active in Alzheimer's brains even with normal thiamine intake.
Treatment evidence is thin.Limits Too few trials exist to set the right thiamine dose for Wernicke–Korsakoff, and thiamine has not been shown to help Alzheimer's. A small trial of benfotiamine (a thiamine pro-drug) slowed one Alzheimer's measure but not the main one. The warning that glucose before thiamine triggers Wernicke's rests mainly on case reports; give both, without delaying glucose.
Ageing
Glucose use falls with age, most clearly in the frontal lobe (prefrontal and anterior cingulate cortex), not fully explained by shrinkage.
The "growth" part goes first. In 205 healthy adults aged 20–82, aerobic glycolysis — fast glucose use that supports growth and plasticity — declined steadily, more than oxygen use.
Mitochondria slow down. In ageing rodent brains, respiration and the activity of complexes I and IV fall by roughly a quarter to a third.
Ketones still work. Older adults took up less glucose than young adults, especially in the frontal cortex, but the same amount of the ketone acetoacetate; in mild cognitive impairment and early Alzheimer's glucose use falls further while ketone use holds.
Part of the "decline" may be less tissue.Limits In carefully screened healthy men, the drop disappeared after correcting for brain shrinkage, and the size of age effects depends on the correction method.
Not enough fuel or oxygen arrives
Sudden sugar drop (hypoglycemia)
Blood glucose falls below about 3 mmol/L — most often from insulin or other diabetes medicine with too little food or extra exercise. Attention, judgement and mood are hit within minutes; very low, long-lasting lows can kill neurons.
Skipping meals and fasting
In healthy people the brain is protected first: the body keeps blood glucose up, and in long fasting the liver makes ketones that can supply most of the brain's fuel.
Low oxygen
High altitude or long-term lung disease; the brain lowers its glucose use to cope.
Slowly reduced blood flow
Narrowed small arteries and a weaker blood–brain barrier reduce delivery over years.
Demand outgrows supply
Sleep loss
After a night without sleep, glucose use falls in prefrontal and parietal cortex and in the thalamus.
Head injury (concussion)
After a blow, neurons need much more energy just as blood flow drops — an "energy crisis" that can last days.
Where these mechanisms lead
The same shortage shows up differently at different ages: a developing brain builds less, an adult brain thinks and copes less well, an ageing brain loses neurons. Empty cells mean no good evidence was found, not "no effect".
Mechanism
In development
In adults
In ageing & neurodegeneration
Sleep loss
Toddlers lose emotional control after a missed nap.
Attention, mood and the prefrontal brake on the amygdala.
Amyloid-β rises about 5 % after one night awake.
Insulin resistance
—
Lower glucose use and poorer memory in type 2 diabetes.
This is basic educational information, not medical advice. If you are worried about any of these, talk to a doctor.
Energy Deficiency
Neuron Impact
Almost every step of a signal costs energy, so a shortage can weaken it in several places. They are not equally sensitive, though. The synapse fails first; the electrical spike itself is one of the last things to go .
The places an energy shortage can act, numbered as in the list below.
1
Do neurons fire less often? Yes — early, partly on purpose
When ATP falls, ATP-sensitive potassium (KATP) channels open and quieten the neuron, a built-in brake that protects it . ATP broken down to adenosine also dampens activity through A1 receptors . In milder, long-term shortage (food restriction in mice) neurons kept their firing rate but saved 29 % of their ATP by using weaker synaptic currents, at the cost of less precise signals .
2
Do they fire with less energy, a weaker spike? Not at first — late
A spike is all-or-none: if it fires, it is full size, because it is powered by the sodium and potassium gradients the pumps have already built up, not by fresh ATP. Only when the pumps fall far behind do the gradients run down; spikes shrink, then stop as the neuron depolarises (depolarisation block). In severe shortage this ends in a wave of complete depolarisation spreading through the tissue .
3
Is the signal re-amplified less well along the axon? Sometimes — long, thin or fast-firing axons
The spike is regenerated at every node of the axon by sodium channels, and the pumps there must clear the sodium afterwards. Long axons get part of their fuel from the myelin-making oligodendrocytes and can bridge short gaps with glycogen from astrocytes; once that is used up, conduction fails . Failures show up first at high firing rates and at thin branch points.
4
Do synapses release less effectively? Yes — the first thing to fail
In low oxygen or blood flow, synaptic transmission stops while the neurons themselves are still intact; the failure is mainly presynaptic, in transmitter release . This "electrical silence" is reversible if supply returns in time . Adenosine adds to it by turning release down .
5
Do the vesicles regenerate less well? Yes — mainly (a) speed and (c) number
(a) Slower. Pulling vesicles back from the membrane (endocytosis) is the most ATP-hungry step of the vesicle cycle; without local ATP it stalls . In cultured neurons low oxygen cut endocytosis to 44 % and release to 72 % of normal .
(b) Less transmitter per vesicle. Likely, but less directly measured: vesicles are filled by a proton pump (V-ATPase) that runs on ATP and leaks constantly, so filling depends on steady energy .
(c) Fewer vesicles ready. Yes, during sustained activity: when recycling cannot keep up, the pool of ready vesicles runs down and the synapse fatigues .
6
Other effects Clean-up, rhythm, upkeep
Clean-up fails. Glutamate is removed from the synapse by transporters driven by the sodium gradient. In severe shortage they run backwards and release glutamate, overstimulating neurons (excitotoxicity) .
Rhythms go first. Fast-firing inhibitory interneurons are among the most energy-hungry cells; the fast brain rhythms they pace (gamma oscillations, important for attention and memory) are especially sensitive .
Upkeep is postponed. Cells cut "optional" spending such as making proteins before ion pumping , and starved animals switch off costly long-term memory .
Calcium and water. Calcium pumps fall behind and calcium builds up inside; sodium pulls water in and cells swell.
Lower glucose use over years, linked to cognitive decline
Partly — ketones can still be used
Critical (stroke, cardiac arrest)
Not the focus here: supply stops almost completely and neurons die within minutes
—
Impact
Impact: a sharp drop or a long, low supply
How an energy shortage shows depends on how fast it comes. A sharp drop sets off an alarm and changes attention and mood within minutes. A small shortfall that lasts months or years gives no alarm — the brain adapts by doing less, and the cost builds slowly.
Acute
Minutes to hours: low blood sugar, a sleepless night, altitude. Usually fully reversible.
When fuel falls quickly, the parts of the brain we use for attention, self-control and handling emotions slow first. The effects are real, but the evidence is much stronger for some causes (low blood sugar in diabetes, lost sleep) than for everyday hunger.
What the brain does first
The hypothalamus senses even a small fall in blood glucose and its blood flow rises; it starts the counter-regulation that releases stress hormones and makes you hungry. That alarm — shakiness, sweating, a racing heart, hunger — is the body defending the brain's supply.
Energy-hungry higher regions slow down first, while the brainstem and hypothalamus keep working.
In adults
Mood: irritability and anger ("hangry"). Day-to-day hunger goes with more anger and irritability and less pleasure; hunger makes people read situations more negatively, mostly when they are not tuned in to their own feelings.
Attention, judgement and reaction time. True hypoglycemia (about 2.5–3 mmol/L) clearly impairs several kinds of attention and executive function — a known risk when driving.
Emotional control after lost sleep. One sleepless night made the amygdala react about 60 % more to negative images and weakened its link to the calming prefrontal cortex; mood and anxiety worsen reliably.
Coping and empathy. About 56 hours awake lowered emotional intelligence and constructive coping.
Aggression toward a partner. One study linked lower evening glucose to more aggression in married couples — disputed.
Chronic: long, low energy
Thinking and memory
Ageing. Brain glucose use declines with age, and more in people who go on to develop Alzheimer's disease — often years before symptoms.
Diabetes and insulin resistance. People with diabetes have a higher risk of dementia, both Alzheimer's and vascular.
Repeated severe lows. In older people with type 2 diabetes, each serious hypoglycemia episode was linked to a higher later risk of dementia.
Too little sleep, night after night
Sleeping 6 hours a night for two weeks slowly built up attention lapses until they matched one to two nights without any sleep — yet people felt only slightly sleepy and did not notice how impaired they were.
Neurons at risk
Cells with the highest, nonstop energy demand are the first to fail when supply stays low: dopamine neurons of the substantia nigra (Parkinson's disease), and fast-spiking inhibitory interneurons whose loss disturbs brain rhythms.
The brain adapts
Neurons can save energy by turning their synapses down — in food-restricted mice they kept firing but used 29 % less ATP, at the cost of less precise signals. The ageing brain keeps its ability to burn ketones even as glucose use falls, which is why ketones are studied as a "brain energy rescue".
Energy Deficiency
Toddlers and kids
A young child's brain is big for its body and busy building itself. It takes a far larger share of the body's energy than an adult's, from smaller reserves — so the time between meals matters more.
~2×the adult rate of brain glucose use (per gram), from about age 3 to 9
~66 %of resting energy goes to the brain at its peak, around age 5 — about 20 % in adults
2–3 hbetween meals and snacks for toddlers: about 3 meals and 2–3 snacks a day
Why children are different
A hungry, growing brain. Brain glucose use rises above the adult rate by about age 3, stays near twice the adult rate until about 9, and falls to adult levels by the late teens. At its peak, around age 5, the brain takes about two-thirds of the body's resting energy and over 40 % of all the energy it spends — and body growth is slowest at exactly that age, as if the body makes room for the brain.
Small reserves. Children burn glucose faster for their size than adults, and the liver's glycogen store lasts less time — roughly 4–8 hours in infants against 8–12 hours in older children and young adults. Fasting children therefore go low and switch to ketones sooner than adults do.
Smaller stomachs, more frequent eating
A toddler's stomach holds little, so a meal can carry only so much energy. Feeding advice follows from that: offer food or drink about every 2–3 hours — around 3 meals and 2–3 snacks a day — at regular times rather than grazing all day. Appetite also varies a lot from day to day once growth slows after the first year.
Put together — a large brain demand, a small meal and a small reserve — a young child has less margin between "fed" and "running low" than an adult.
Sugary foods and the time between meals
Fast carbohydrates arrive fast and leave fast. Juice, sweets and refined, puffed or flaked starches (rice cakes, cornflakes) have a high glycemic index, close to glucose itself; fat, protein and fibre slow digestion.
They can shorten fullness.Some evidence Children aged 9–12 ate about 145 kcal more at lunch after a high- than after a low-glycemic breakfast. Children aged 4–6 were hungrier before lunch after a high-glycemic breakfast, but ate the same. In 10–12-year-olds, the glucose curves differed but fullness and thinking over 3 hours did not. In teenagers with obesity, a high-glycemic meal led to lower blood sugar hours later, more adrenaline and more eating.
Short-term: mood and behaviour
Lost sleep → tantrums and big emotions. The best evidence. Toddlers who missed one nap showed about a third more negative emotion and less positive emotion. Poor sleep goes with emotional and behavioural problems through childhood.
Hunger → frustration and poorer attention. Plausible and widely said, but thin evidence: one small, old study found a glucose drink late in the school day kept 6–7-year-olds more attentive and less frustrated; breakfast studies are mixed and low quality. No study has measured hunger as a direct tantrum trigger.
Low blood sugar in children with diabetes. After unnoticed night-time lows, next-day mood was worse even though test scores held. Behaviour is an unreliable sign: parents missed more than half of true lows.
Also often reported (less studied): crying and clinginess, trouble switching between activities and poorer focus — the same prefrontal skills that lag when sleep or blood sugar is low.
Building a brain costs energy
Childhood is when the brain wires itself. Synapse numbers peak in childhood — earliest in the visual and hearing areas, latest in the prefrontal cortex, which keeps pruning into the teens. The peak in brain energy use falls in the same years as the peak in synapses. Part of a child's glucose is not burned for ATP at all but used as building material (aerobic glycolysis), in step with the genes for growing synapses and myelin. Learning itself is costly too: new connections need energy to build and keep — see Neuroplasticity.
Does long-term low energy affect development?
For severe or specific shortages, yes. For everyday mild shortfalls, it has not been shown.
Mitochondria impairment Strong
Not rare in children. Disorders of the mitochondrial energy chain that start in childhood affect at least 1 in about 20,000 children, and about 1 in 7,600 people at any age.
The brain is hit first. In children these disorders usually involve the brain — developmental delay or loss of skills, low muscle tone, seizures — because it is the most energy-hungry organ. Mitochondrial disease is a common cause of neurological illness in childhood.
Earlier start, worse course. In 73 children, 90 % had neurological signs; symptoms starting before 6 months was the strongest predictor of a poor outcome, while those starting later mostly kept their independence.
Leigh syndrome. The most common childhood form (about 1 in 40,000 births), with more than 75 known genes: a progressive loss of skills with lesions in the basal ganglia and brainstem. Median onset is 7 months, and 81 % start by age 2.
Illness and fasting set off setbacks. Fever, infection, prolonged fasting or dehydration can tip a child into an energy crisis with lasting regression, so care standards say to avoid long fasts and to give glucose during illness.
Mitochondria set the pace of brain building. Human neurons mature slowly partly because their mitochondria are slow; boosting mitochondrial metabolism made them mature faster, and lowering it slowed mouse neurons. Mitochondrial shape also steers whether neural stem cells keep dividing or become neurons.
Synapses need local mitochondria. Fewer mitochondria in dendrites meant fewer spines and synapses; more meant more. Mitochondria parked next to synapses power the protein-making that plasticity needs.
Shared with intellectual-disability conditions. Weaker energy production and more oxidative stress are found in Down, Rett and Fragile X syndromes, where they may hold back neurogenesis and plasticity.
Low blood sugar after birth Moderate
Newborns with a single early glucose below 35 mg/dL were less often proficient in literacy (32 % vs 57 %) and maths (46 % vs 64 %) in fourth grade.
Babies who had neonatal hypoglycemia had about twice the rate of low executive-function scores at 4.5 years (10.6 % vs 4.7 %), mostly after severe or repeated lows.
A meta-analysis of 11 studies: more visual-motor and executive problems in early childhood, and more learning problems in mid-childhood.
Symptomatic lows can injure white matter (often at the back of the brain), with later impairment in many of the infants.
But in a large, carefully treated cohort, school achievement at about 9 years did not differ — prompt treatment of mild lows may prevent harm.
Thiamine (B1) deficiency in infancy Moderate
Thiamine is needed to burn glucose. In 2003 a soy formula without thiamine caused severe deficiency in Israeli infants; two died.
Infants exposed without severe illness had delayed language, lower mental development scores and later walking at about 2½ years.
Of the survivors of severe deficiency, 7 of 8 had intellectual disability and 6 developed severe epilepsy.
Thiamine deficiency still causes infant deaths where diets rely on polished rice, and even mild deficiency may affect development.
Iron deficiency in infancy Moderate
Iron is part of the mitochondrial energy chain. In iron-deficient newborn rats, cytochrome c oxidase activity fell by up to 42 % in the hippocampus and cingulate cortex.
In developing neurons, iron deficiency lowered both mitochondrial respiration and glycolysis and gave fewer dendrite branches.
Ten years after treatment, children who had severe iron deficiency as infants did worse at school and had more behaviour problems; at 25 years they had about one year less schooling.
Iron also builds myelin and dopamine, so this is not energy alone; the effects outlast treatment.
Long-term under-nutrition Moderate
More than 200 million children under 5 in low-income countries are estimated not to reach their developmental potential, with stunting closely tied to poorer thinking and schooling.
Shortfalls of energy, protein, iron, iodine, zinc and omega-3 fats in the first ~1000 days disturb neuron growth, myelination and synapse formation.
Malnutrition at age 3 predicted more aggression and hyperactivity at 8 and conduct problems at 17, partly through lower IQ.
In Barbados, adults malnourished as infants had lower IQ and more attention problems 40 years later.
DHA deficiency Moderate in animals, mixed in children
A building block, not a fuel. DHA (an omega-3 fat) piles up in the brain and retina in the last months of pregnancy and the first two years.
Linked to brain energy. In rats low in omega-3, brain glucose use fell by about 30 % in several regions, and the glucose transporter GLUT1 at the blood–brain barrier dropped by 25–30 %.
The brain needs its own DHA transporter. Mice lacking it (Mfsd2a) have small brains and lose neurons; children with broken MFSD2A have microcephaly and intellectual disability.
Low intake in animals harms neurogenesis, learning and vision.
Supplements in healthy children: mixed. DHA in pregnancy did not raise IQ at 18 months or 7 years; DHA formula did not change 18-month scores across 15 trials, though one trial found better rule-learning and vocabulary at 3–5 years.
Plasticity on a budget Plausible, untested in children
Long-term memory needs extra energy: flies forming it roughly double their sugar intake, and the energy rise in memory neurons is needed for memory to form.
When energy is short, animals cut the costliest plasticity first: starved flies switch off long-term memory, and food-restricted mice weaken their synapses.
In a growing brain the same saving could slow wiring — an inference, not a finding.
Impact · outside the main focus
Critical energy loss
Sometimes the brain's supply is cut off suddenly and almost completely. These are medical emergencies, and they work very differently from the gradual shortages the rest of Brain Energy is about.
!
Not the focus of this site. Brain Energy is about everyday and long-term energy shortage. This page only outlines critical events so they are not confused with it. In an emergency, call your local emergency number.
What counts as critical
Stroke
A blocked or burst artery cuts off part of the brain. In a major stroke about 1.9 million neurons die every minute until blood flow returns .
Cardiac arrest
The heart stops and supply to the whole brain ends; consciousness is lost within about 10 seconds .
Suffocation and poisoning
Choking, drowning or carbon-monoxide poisoning stop oxygen reaching the brain.
Hypoglycemic coma
Very low blood sugar for a long time can kill neurons in the cortex and hippocampus .
Why it is different
In gradual shortage the brain has time to adapt: it turns firing and synapses down, switches fuel and protects vital regions. In a critical event there is no time. With almost no fuel stored, synapses go silent within seconds, and if blood flow stays very low the pumps stop altogether .
Blood flow (normal ≈ 50 mL per 100 g per minute)
What happens
Reversible?
Below ~20
Synapses stop transmitting, EEG goes flat; neurons are silent but intact
Yes, if restored in time
Below ~10
Pumps fail, neurons depolarise in spreading waves, glutamate floods out, calcium builds up
No — neurons die within minutes
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Configuration Options
Colour of every region. Sub-regions start from their own colour, so change them one by one.
