Two people are rear-ended at the same intersection, at the same speed, on the same afternoon. Same airbags, same whiplash, neither of them blacks out, both get a normal CT. Six weeks later one is back at work and the other is still cancelling meetings because the screen makes her nauseous. The crash was identical. The brains were not.
The injury is an energy crisis
A concussion is not a bruise. In the first seconds, stretched membranes dump potassium out of cells and let calcium in, glutamate floods the space between them, and the brain’s ion pumps start working furiously to restore order. Those pumps run on ATP. So demand for glucose spikes sharply — at exactly the moment cerebral blood flow typically falls.
The literature calls the gap that opens a metabolic crisis. It is the reason a concussed brain gets tired doing things that used to be free, and the reason symptoms come on when you read a screen: load raises an energy demand the tissue currently cannot fund. We cover the mechanism in detail on what a concussion actually does to the brain.
Hold that thought, because it reframes the whole question. If the injury is fundamentally a problem of energy supply and demand, then how well your metabolism worked the day before the crash is not a side issue. It is part of the injury.
Giza CC, Hovda DA. The New Neurometabolic Cascade of Concussion. Neurosurgery. 2014;75(Suppl 4):S24–S33. doi:10.1227/NEU.0000000000000505
The injury makes the brain insulin resistant — and a bad terrain makes that worse
Here is where it stops being theoretical. Researchers examined what a brain injury does to insulin signalling, which is the system that gets fuel into brain cells.
They found that traumatic brain injury induces acute insulin resistance in the brain. After a single injury it resolved within about seven days. After repeated injuries it persisted for twenty-eight. So the injured brain temporarily loses some of its ability to respond to the very signal that would help it take up fuel and damp inflammation — during precisely the window when it needs both most.
Then they added the variable that matters here. Obesity — which already causes brain insulin resistance and neuroinflammation before any injury occurs — made the consequences of the brain injury worse. The animals carrying that metabolic burden showed prolonged disruption of insulin signalling, more microglial activation, and measurable deficits in learning, memory and anxiety-like behaviour.
Be clear about the evidence tier: that is a mouse study, not a clinical trial. It does not license a promise that changing your diet will fix post-concussive symptoms, and we are not making one. What it does is describe a mechanism that is coherent, measurable, and consistent with what we see in the clinic — two people, one crash, two different recoveries.
Karelina K, Sarac B, Freeman LM, Gaier KR, Weil ZM. Traumatic brain injury and obesity induce persistent central insulin resistance. Eur J Neurosci. 2016;43(8):1034–1043. doi:10.1111/ejn.13194
The terrain most American adults bring to a crash
The pattern of eating that dominates in this country — refined carbohydrate, industrial seed oils, ultra-processed food, very little fibre — does not announce itself as a brain problem. It announces itself, if at all, as a waistline or a lab value. But the same pattern is associated in the literature with insulin resistance, chronic low-grade inflammation, and vascular changes that reach the brain, and reviews of dietary patterns and cognitive decline keep landing on it as a modifiable contributor to how the brain ages.
Most people carrying that terrain feel fine. That is the point. It is not a disease you are aware of having — it is a reduced margin. And a reduced margin is invisible right up until something demands a surge of capacity you no longer have.
A concussion is exactly that demand.
Why this keeps getting missed
Almost everything known about concussion recovery comes from studying young athletes: healthy, monitored, identified within minutes, and metabolically about as good as humans get. Those studies systematically exclude people with diabetes, obesity, sleep apnoea and vascular disease.
Which means the recovery timelines the whole field quotes — and that get quoted back to patients — were established in the population least like the middle-aged adult who was rear-ended on the way home from work. When that person does not recover on schedule, the conclusion drawn is usually that they are exaggerating. The more parsimonious conclusion is that the evidence base never included them.
See the long-term effects of concussion for what the outcome data actually show, including where the published figures disagree.
What we do about it
Treating the terrain is not a substitute for treating the injury. The vestibular and oculomotor work is what resolves the dizziness and the visual intolerance, and nothing nutritional replaces it. But we assess and treat the metabolic side alongside it rather than handing it to somebody else, because it is part of the same problem:
- Glucose handling and insulin resistance — the system the injury has just disrupted centrally
- Sleep, including sleep-disordered breathing — no amount of rehabilitation outruns a brain that is intermittently hypoxic all night
- Inflammatory load — the injury adds neuroinflammation to whatever was already running
- Simple fuelling during recovery — the unglamorous point that an injured brain with elevated glucose demand should not be running on skipped meals
Details on the clinical side are on treatment.
If this idea is the interesting part
The argument on this page is narrow: it is about concussion, and about why two people with the same crash get different outcomes. But the underlying idea is bigger than head injury. Cognitive decline in general looks far less like a disease that arrives one day and far more like a terrain that gives way gradually — energy, vasculature and inflammation failing quietly, for years, long before anyone calls it a diagnosis.
Dr. Padda wrote a book about that: The Starved Brain. It is not about concussion, and it is not a companion to this clinic — it is a separate, editorial argument about cognitive decline as a metabolic and structural failure rather than an inevitability of age. If the terrain idea is the part of this article that stayed with you, that is where it is developed properly.
Read about The Starved Brain →
If you are in the St. Louis area and the reason you are reading this is a head injury that has not resolved, that is a different conversation and a clinical one — start here.
The short version
- A concussion is fundamentally an energy crisis in brain tissue, not a bruise.
- Brain injury induces insulin resistance in the brain itself — briefly after one injury, for far longer after repeated ones.
- In animal work, a pre-existing metabolic burden made the same injury worse: more inflammation, more memory deficit, slower recovery.
- The trials that set expectations for recovery excluded the people most likely to be carrying that burden.
- So the honest answer to “why am I not better yet?” is often not that the injury was worse. It is that the ground it landed on was.