This chapter asks a simple but thrilling question: did life’s oldest network builders—fungi—help nudge animals toward intelligence? Not by “donating a brain,” and not through a hidden endosymbiosis that left no trace, but by sharing a world so closely with early animals that it biased how those animals sensed, learned, and coordinated their actions.

Two ideas guide the story. First, fungi and animals inherit the same ancient eukaryotic parts for building living systems—polarity, scaffolds, and traffic for moving membranes and messages. Given similar pressures, both lineages discovered similar ways to run a network: grow in a direction, deliver cargo where it matters, and integrate local signals. Think of this as convergent operational logic, not a shared organelle or a borrowed set of “neuron genes.” On present genetic evidence, a direct fungal ancestry for animal neurons is unlikely.

Second, intimacy changes things. For hundreds of millions of years, early animals—tiny worms among them—lived inside fungal landscapes: eating, being eaten, dodging traps, following scents, and marinating in fungal chemistry. That contact likely trained receptors, tuned neuromodulators, and rewarded quick learners. In effect, this was the original gut–brain axis: what the body touched and ate (fungal cues, nutrients, irritants) pushed nervous systems into the right states (explore, conserve, avoid), and those states fed back into what the body sought next. Intake shaped state; state shaped intake. Influence, not inheritance.

Along the way we’ll keep the tone plain-spoken and the claims testable. We’ll begin with fungi—not as mystic sages, but as quietly brilliant engineers of conduit-based computation. Then we’ll zoom in on nematodes, nature’s simplest successful animals, to see how close contact with mycelial worlds might have encouraged small brains to get a little smarter.

A cultural aside: readers may recall the “stoned ape” idea in humans. We cite it here as analogy, not evidence—a reminder that chemical ecologies can shape minds—while our focus stays on mechanisms we can actually test.

1.1 Why start with fungi?

Before brains, there were networks. By around 1.0–1.5 billion years ago, fungi (or fungus-like lineages) were already experimenting with life as a living web—miles of mycelium stitched through substrates, quietly moving water, minerals, and messages. The fossil and molecular hints here aren’t perfect, but they consistently place early fungi deep in deep time.

These networks don’t think like we do, but they coordinate, prioritize, and adapt—the basic verbs any intelligence depends on. A hyphal tip pushes forward, chooses a path, and adds membrane exactly where growth is needed. Packets of cargo stream to the tip; signals ripple back through the network; branches strengthen or wither based on results. If that sounds familiar, it should. Animal neurons also extend processes, traffic cargo to hot spots, and adjust connections according to experience. The parts are ancient and shared across eukaryotes; the architecture—how those parts are arranged and regulated—differs by lineage, yet lands on a similar control logic.

What about animals? The first clear bilaterian animals—the “worm-like” body plan most lineages build from—show up in the late Ediacaran, about 560–555 million years ago (for example, Ikaria wariootia). There are controversial claims of worm-like traces closer to ~1.0–1.1 billion years ago, but those remain debated and haven’t displaced the mainstream timeline. The safe takeaway is that fungal networks were likely established hundreds of millions of years before unambiguous bilaterian worms.

Does that mean neurons descended from hyphae? No. If fungi had bequeathed animals their neural hardware through a hidden endosymbiosis, the genomes should tattle; so far, they don’t. The better story is less romantic and more interesting: given the same kit and similar problems, life keeps rediscovering workable designs.

So we begin underground, where signal follows conduit and decisions are distributed. Fungi show you can run a vast, responsive network without a head office. When animals finally arrive on the scene, they don’t copy this blueprint—they translate it: taking the logic of directional growth, targeted delivery, and local integration and applying it to moving bodies and fast reactions. That is where intelligence starts: not as a bolt from the blue, but as an upgrade of network craft already proven in other forms of life.

1.2 Nematodes: first stop on the animal road to mind

If you want to watch intelligence emerge without getting lost in billions of neurons, study a creature with 302 of them. Nematodes—tiny roundworms that thread through soils, roots, and rotting wood—are the perfect lens. They are everywhere. They are simple enough to map completely, yet clever enough to learn: to follow a scent, avoid a trap, and change their habits when the world changes.

Crucially, nematodes make their living inside fungal neighborhoods. Some nibble hyphae. Some get hunted by predatory fungi that build living lassos. Some share cues with fungi about food and danger. In such a neighborhood, a worm’s survival depends on reading a dense chemical conversation—indoles, volatiles, peptides, ions—and using that information quickly. Animals that sensed better and adapted faster had the edge.

It isn’t hard to imagine the feedback loop. Fungi sculpt the landscape with nutrients and signals. Worms track those patterns, and the best trackers leave more descendants. Over time, receptors diversify, neuromodulators settle into useful ranges, and tiny circuits learn a little faster. No one needed to transfer a “neuron gene” from fungus to worm; the pressure of living together was enough to push simple nervous systems toward smarter behavior.

This is the spirit of the chapter. We won’t ask you to memorize molecular pathways. We’ll keep our eye on the operational moves that matter across life: grow toward value, route resources to where they count, and integrate signals locally so the next move is better than the last. Fungi did that as distributed webs. Nematodes began doing it with spiking cells and tiny circuits. From there, bigger bodies and richer societies would scale the same logic into something we now call intelligence.

1.3 Contact zones: fungivory, parasitism, and chemical ecologies

Walk through a handful of soil and you’re holding a crowded city. Filaments of fungus thread every direction; tiny roundworms slide between them like commuters in a rush-hour maze. In this city, fungi and animals don’t just bump into each other—they live off, hunt, outsmart, and sometimes support each other. Those contact zones are where small nervous systems get stress-tested, refined, and, over time, made a little smarter.

Fungivory: when worms eat the web

Many nematodes are simple opportunists: if a hypha crosses their path, they nibble. For the worm, that means tracking where the good stuff is and when it’s worth the risk. For the fungus, it means either tolerating a bit of grazing or defending the network. This everyday nibble-and-respond dance matters because it rewards animals that can sense gradients, remember spots, and adjust tactics. Even a minimal brain gets better when the map of “smell → reward” becomes sharper.

Think of a worm learning that one fungal scent leads to calories while another hints at moldy trouble. Follow the first, avoid the second. That tiny upgrade—turning raw chemical noise into a simple rule of thumb—is intelligence in embryo.

Parasitism: when the web fights back

Fungi are not passive salad. Some build living lassos or adhesive traps that snare passing worms. Others invade animal cells from the inside. From the worm’s point of view, this is selective pressure with teeth. Miss a cue, and you’re lunch.

Predators like these are nature’s examiners: they punish sloppy sensing and slow decisions. Worms that twitch away from a trap at the right moment survive; worms that don’t, don’t. Over generations, that pressure can tune the gears that matter—faster detection, cleaner signal-to-noise, better learning from near-misses. You don’t need many neurons to show improvement; you just need the right ones to re-weight their responses after each encounter.

Chemical ecologies: the shared language of the neighborhood

Soil is a conversation. Fungi release clouds of molecules—indoles, volatiles, small peptides, ions—that advertise food, danger, crowding, or territorial lines. Nematodes read that chemical weather with an expanding toolkit of receptors. Some cues attract, some repel, some modulate mood-like states (stay, explore, flee).

What matters here isn’t memorizing names of molecules. It’s the logic: the same signal can mean different things in different contexts; mixtures matter more than single notes; timing changes the message. Nervous systems that can learn these patterns—by strengthening useful links and weakening useless ones—do better. Over time, families of receptors can expand and specialize, and neuromodulators can slide into stable “set-points” that fit the local soundtrack. That’s how a neighborhood writes itself into a nervous system without transferring a single gene: repeated exposure shapes what’s worth noticing.

From conflict to cooperation: the mutualism edge

Not every encounter is war. Sometimes fungi and worms settle into mutual convenience. Fungi restructure soil and ferry nutrients; worms aerate channels and spread spores. Even loose, opportunistic mutualisms create positive feedbacks that reward coordination. Animals that can predict a friendly fungus’s patterns—or at least avoid tripping its alarms—waste less energy and take fewer risks. Small brains save effort by internalizing the rhythms of their partners.

Why these contact zones matter for intelligence

Put it all together and the path is clear:

• Fungivory trains animals to track resources and update simple maps of “what pays.”
• Parasitism trains speed, attention, and learning from close calls.
• Chemical ecologies train pattern recognition across messy mixtures and shifting contexts.
• Mutualisms train long-horizon coordination and energy efficiency.

None of this requires borrowing “neuron genes” from fungi. It requires living together—long enough and closely enough that the worms with slightly better sensing, slightly better weighting of signals, and slightly better memory keep winning. Intelligence doesn’t need a lightning bolt; it needs a neighborhood that rewards brains, even tiny ones.

1.4 Shared toolkit → convergent operational logics

Here’s the big idea in friendly terms: fungi and animals were issued the same starter kit when eukaryotic life first assembled its basic machinery. Think of it as a box of universal parts—compasses that tell a cell which way is “forward” (polarity switches), scaffolds that push and pull (actin and microtubules), conveyor belts for moving cargo, and docking stations for fusing new membrane into place. Different lineages didn’t invent brand-new parts from scratch; they recombined the same parts in different ways.

Now add the problem both had to solve: run a living network efficiently.

• You need to grow in a direction (toward sugar in wood, or toward a signal in tissue).
• You need to deliver cargo exactly where it matters (cell wall material at a hyphal tip; receptors and vesicles at a budding synapse).
• You need to integrate local signals so the next move is better than the last (strengthen a branch that pays off; weaken one that doesn’t).

Fungi did this as a distributed web. A hyphal tip is like a forward operating base: the network steers growth there, feeds it with streams of packets, and adjusts branches depending on feedback from the environment. Animals translated the same logic into neural craft. A neuron extends a dendrite, routes molecular traffic to hotspots, and tunes connections up or down based on experience. Same three moves, different stage.

If we open the box and label the pieces, the parallels get clearer without getting technical:

• Orientation → a “this-way” switch that biases growth to one side.
• Scaffolding → flexible struts that can push, pull, and stabilize.
• Logistics → belts and tethers that carry parcels to the front.
• Docking → zipper-like proteins that let parcels fuse and unload.
• Local rules → simple updates: “more of what worked, less of what didn’t.”

Put together, those pieces form what we’ll keep calling convergent operational logic: polarized outgrowth + targeted delivery + local learning. It’s not that neurons descended from hyphae; it’s that both discovered the same winning playbook because they started with the same parts and faced similar constraints.

Why this doesn’t imply hidden gene transfer: if fungi had literally donated key “neuron genes” to animals, we’d expect tell-tale genetic fingerprints. What we actually see (from comparative biology) is that these core parts are older than both fungi and animals, and each lineage built its own high-level architecture on top. In other words, the hardware was shared from the beginning; the software—how the parts are orchestrated—evolved separately.

The takeaway for our story is practical. We don’t need to hunt for a mythical fungal brain hiding in animal DNA. We need to pay attention to how similar network chores were solved on two sides of the tree of life, and how living side-by-side in the same neighborhoods might have nudged animals to adopt—and then turbocharge—the same control logic. That’s the bridge from mycelial webcraft to mind.

1.5 Two routes this story could have taken

There are two clean ways to tell a “fungus shaped animal intelligence” story. One is a shortcut; the other is slow influence. We’ll take them in turn and be plain about what the evidence would need to show.

Route A — The shortcut: ancestry by merger (endosymbiosis/HGT)

The attraction. We’ve seen mergers change life before. Mitochondria were once free-living bacteria; their capture turbocharged eukaryotes. So it’s tempting to imagine a similar event: fungi “donate” neural know-how to early animals—maybe even a small genetic toolkit for outgrowth and signaling—and intelligence gets a head start.

What the genomes would say if that happened.
If fungi had handed animals key neural parts, the record would be hard to hide. We’d expect:

• Animal “neuron genes” that nest inside fungal families on evolutionary trees.
• Islands of foreign-looking genes clustered near neural regions (a telltale of gene packages moving together).
• Odd accents in the DNA—different intron patterns, GC content, or neighborhood quirks that look more fungal than animal.

What we actually see.
Plenty of shared parts—because fungi and animals both inherited the same ancient eukaryotic kit—but not the fingerprints of a later fungal handoff. The high-level wiring for hyphae and for dendrites looks like two independent builds using the same toolbox.

Where that leaves Route A.
A neat idea, but on present evidence unlikely as the main story. Still: if new data ever showed a genuine fungal “island” parked in an animal’s neural genome, or a core dendritic regulator sitting inside a fungal clade, we’d change our minds. Until then, treat this as a falsifiable foil, not the headline.

Route B — The long game: influence by living together (parasitism → mutualism)

The attraction. You don’t have to swap genes to shape minds. You just have to share a world long enough and intimately enough that the winners are those who sense it better and learn faster. Early animals, especially nematodes, lived in fungal neighborhoods thick with signals—scents, tastes, ions, defensive sprays, lures.

How this could push brains forward.

• Receptor training: Animals evolve more—and more finely tuned—receptors for the chemical “weather” fungi create.
• Neuromodulator tuning: Repeated exposure sets the “mood knobs” of tiny nervous systems (when to explore, when to hunker down).
• Learning shortcuts: Circuits that quickly re-weight their responses after close calls or payoffs get copied to the next generation.

What the world would look like if this were true.

• Worms and other small animals would read fungal neighborhoods with surprising sophistication.
• Families of sensory receptors would expand in lineages that live cheek-by-jowl with fungi.
• Long exposure to specific fungal cues would leave heritable dents—subtle shifts in gene regulation and behavior that don’t require new genes, just new weights on old ones.

What we actually see.
Exactly the kind of contact zones that reward better sensing and faster learning: fungivory, fungal predation, chemical cross-talk, and even loose mutualisms. It’s not proof on its own—but it’s the right kind of pressure to make mini-brains smarter without borrowing parts.

Where that leaves Route B.
This is the working hypothesis: influence, not inheritance. It fits the genetics (no need for a hidden merger), matches the ecology (constant contact), and gives us experiments to run.

A quick cultural aside

People sometimes ask about the “stoned ape” idea in humans—the suggestion that psychoactive fungi nudged hominin cognition. We mention it here as analogy, not evidence. Our focus is more basic and more ancient: not on altered states in primates, but on everyday chemical ecologies training tiny nervous systems over evolutionary time.

What would change the story?

Science moves forward by making it easy to be wrong. Here’s our open invitation to future data:

• To upgrade Route A (ancestry): show us a bona fide fungal “gene island” embedded in animal neural DNA, or a core dendritic regulator that resolves inside a fungal family across multiple analyses.
• To downgrade Route B (influence): run controlled exposure experiments and find no heritable changes in receptor families, no behavioral canalization, and no selection signals—despite strong, long-term fungal contact.

Until either happens, the slow, lived-together route remains the best bet: fungi didn’t give animals their brains; they gave them a neighborhood that rewarded brains. Ready to see how that influence could actually work under the hood? Next up: the mechanistic pathways—receptors, neuromodulators, metabolism, and plasticity—translated into plain English.

1.6 How fungi could actually push brains forward

If Route B is our working story—influence by living together—what are the levers? Four simple ones: the locks on the cell’s surface (receptors), the brain’s chemical dials (neuromodulators), the fuel bill (metabolism), and the wiring rules (plasticity).

1) Receptors: learning to read the neighborhood

Think of receptors as locks on the outside of a neuron (or sensory cell). Fungi fill the air and soil with keys: scents, small molecules, peptides, ions. Early animals that evolved a few extra locks—or slightly better versions of old locks—could read that chemical weather more clearly.

• What exposure does: If a certain fungal scent reliably means “food nearby” or “trap ahead,” animals with locks tuned to that scent get paid. Over generations, families of locks expand and specialize.
• What “smarter” looks like here: Not a bigger brain, just a better front end. Finer discrimination, fewer false alarms, faster orientation.

Picture it: a worm with a few more locks for “safe fungus” keeps finding calories; its cousin without them wanders. Intelligence can start at the sensor, long before we talk about thoughts.

2) Neuromodulators: setting the dials for action

Inside even tiny nervous systems are dimmer switches—chemicals that set the mood of a circuit: explore vs. hunker down, risk vs. caution. Fungal neighborhoods nudge those dials all the time.

• What exposure does: Repeated encounters with certain fungal cues can push these dials toward useful set-points—a bias to keep searching when a good fungus is around, or to snap into caution when a trap-building fungus is common.
• What “smarter” looks like here: Better state switching. The animal moves through the world with more appropriate defaults—saving energy and avoiding dumb mistakes.

Everyday analogy: coffee in the morning, chamomile at night. Same you, different mode. For tiny animals, fungal chemistry can do the nudging.

3) Metabolic economics: paying for smarts

Brains are expensive. Even a small upgrade—an extra circuit here, a sturdier memory there—costs fuel. Fungi influence that budget two ways.

• As food: Some fungi are dense packages of nutrients. Access to them can bankroll a little more neural tissue or a little more activity.
• As threat: Predatory or toxic fungi raise the cost of errors. When mistakes are pricey, selection favors animals that invest in better sensing and faster decisions.

Net effect: A landscape that sometimes pays well and sometimes punishes hard rewards efficient intelligence—not necessarily more neurons, but better ones doing the right work at the right time.

4) Plasticity: changing the rules after each encounter

Plasticity is the nervous system’s simple rule: do more of what worked, less of what didn’t. It’s how experience leaves a fingerprint.

• What exposure does: In a fungal-rich world, the feedback is constant. Follow this scent, get food; touch that filament, get stuck. Circuits that reweight themselves after each result quickly become more accurate maps of the neighborhood.
• What “smarter” looks like here: Tiny networks that learn faster and forget noise. Same number of cells, better settings.

Important twist: You don’t need new genes for this; you need new weights on existing circuits. That’s why influence can be powerful without leaving a big genetic signature.

Putting the four levers together

These levers don’t act alone. A better lock makes the signal clearer; tuned dials make the animal responsive; a favorable budget lets it afford the response; and plasticity locks in what worked. Over many generations, this loop ratchets forward: sharper sensing → better states → smarter choices → more descendants → tiny anatomical refinements that stabilize the gains.

And notice what’s not required: a hidden gene transfer from fungi, or a secret endosymbiosis. Living side-by-side is enough.

7. Predictions & simple experiments

If fungi shaped small animal minds by living together (our Route B), the world should look a certain way. Here are clear predictions and easy-to-imagine tests. Each one can move the story forward—or knock it down.

Prediction 1 — “Better locks” where fungi are thick

Claim: Animals that live in fungal-rich habitats evolve more (and more finely tuned) receptors for fungal cues.

Simple test:
Raise lots of nematodes for many generations in two soil microcosms:
A) rich in one friendly fungus; B) poor in fungi.
Every few generations, give the worms a scent choice test (a Y-maze with fungal smell on one side, plain air on the other). See if Line A becomes quicker and more accurate at picking the fungal side—and whether their offspring keep that edge.

What would count as support: faster, cleaner choices in Line A, persisting across generations.
What would hurt the idea: no difference after long exposure, or gains that vanish immediately in offspring.

Prediction 2 — “Mood dials” get tuned by neighborhood chemistry

Claim: Repeated exposure to fungal cues shifts the default state of tiny nervous systems (explore vs. caution).

Simple test:
Expose worms daily to low, safe doses of a friendly fungus’s scent for two weeks. Then put them in a new arena with faint food signals and mild threats. Do they explore more boldly than controls? Do they switch states faster (bold ↔ cautious) when the scene changes?

Support: exposure-trained animals explore more when it pays and hit the brakes quicker when it doesn’t.
Against: no change in default behavior or switching speed.

Prediction 3 — Learning ratchets up under danger

Claim: Predatory fungi (lassos, sticky traps) speed up learning—survivors get better at spotting micro-cues.

Simple test:
Alternate safe and predator days. Measure near-miss learning: how many trials before worms avoid the trap zone reliably? Compare to worms with the same schedule but no predators.

Support: fewer trials to learn; fewer repeat mistakes next day.
Against: learning rate unchanged despite real predation risk.

Prediction 4 — A good fungus bankrolls tiny brains

Claim: Access to nutritious fungi supports small upgrades in neural performance (without adding neurons).

Simple test:
Feed one line a high-quality edible fungus, another standard lab diet. Run a dual-task test: find food while avoiding a mild deterrent. Look for faster decisions and fewer wrong turns in the fungus-fed line.

Support: better performance tied to better fuel.
Against: no performance difference despite extra calories.

Prediction 5 — Experience leaves a heritable dent (without new genes)

Claim: Long exposure to a “fungal soundtrack” leaves tiny, inherited shifts in how circuits are tuned.

Simple test:
Raise grandparents and parents with a specific, harmless fungal scent mix. Test the grand-offspring that grow up without those scents. Do they still orient faster to that mix? (Think of it as a faint behavioral “accent” passed down.)

Support: a small but real advantage that persists one generation.
Against: no trace once the immediate exposure stops.

Prediction 6 — Friendly partnerships save effort

Claim: In mixed communities, worms and certain fungi drift toward low-friction coexistence that rewards coordination.

Simple test:
Build tiny soil “towns” with worms, food sources, and either (a) a neutral fungus or (b) a gently helpful one (e.g., one that concentrates nutrients). Track energy spent per meal (distance, time) and risky encounters.

Support: mutualist towns produce worms that get fed with fewer risks/steps.
Against: no efficiency gain despite the fungal helper.

One “genome treasure hunt” (the ancestry shortcut, just in case)

If the shortcut (Route A) ever happened, we should be able to catch it on paper.

Straightforward screen:
Search animal DNA for tiny “foreign islands”—clusters of genes sitting together that look more fungal than animal—and ask whether any are tied to neural functions. If someone finds a genuine island, repeatedly confirmed, that would upgrade Route A from foil to contender.

Field-trip versions

• The smell maze: Petri dish Y-mazes with a drop of fungal odor on one arm. Count choices over a week of “training.”
• Predator perimeter: A small ring of nematode-trapping fungus; how quickly do worms learn to skirt the edge?
• Mood-switch box: Alternate “rich” and “lean” odor days; watch how quickly worms flip between explore and conserve.

(These are demos—real studies need careful controls—but they make the logic tangible.)

What results would really move the needle?

• Big win for Route B: Long-term exposure lines that show (a) faster orientation to specific fungal mixes, (b) better state switching, and (c) tiny inherited behavioral shifts—without any new neurons added.
• Big win for Route A: A verified fungal gene island embedded near animal neural genes, or a core “dendrite program” gene that sits inside a fungal family across multiple analyses.

Built-in falsification

This framework is only worth keeping if it’s easy to break.

• If exposure doesn’t speed learning, doesn’t bias states, and leaves no heritable impressions—despite heavy fungus contact—Route B weakens.
• If careful genomic hunts never turn up even a single credible fungal island tied to neural function, Route A stays in the “nice story, not our story” box.

1.8 What this means for vertebrates—and for us

So far we’ve stayed small on purpose: fungi as network-builders; nematodes as our first animals with minds you can hold in a thimble. But principles scale. If living alongside fungi can tune tiny nervous systems, what happens as bodies get bigger, diets change, and social lives appear?

Scaling the same three moves

Vertebrates didn’t change the basic playbook; they amplified it.

• Polarized growth → developing brains that wire long-range highways and fine local streets.
• Targeted delivery → synapses that can stock, restock, and modulate on demand.
• Local learning → circuits that strengthen useful paths and prune the rest.

Bigger bodies bring new constraints (temperature control, long gestations) and new opportunities (memory, planning, cooperation). But the logic—grow toward value, route resources where they matter, integrate signals locally—stays put.

The fungal neighborhood doesn’t vanish

We don’t leave fungi behind when we become fish, lizards, birds, or mammals. We share ecosystems, food webs, and—inside us—microbial neighborhoods that include fungi (the mycobiome). For vertebrates, fungal influence shifts from soil-level to dietary, environmental, and internal:

• Dietary: Some fungi are rich, digestible food; others defend themselves with chemistry animals must learn to avoid—or sometimes cleverly use.
• Environmental: Forests, caves, and soils carry fungal “weather” that shapes foraging and risk.
• Internal: Our guts host fungi among bacteria; immune systems learn when to tolerate and when to react. That crosstalk feeds back into mood, motivation, and energy.

None of this implies that fungi “designed” vertebrate brains. It means we grew up in their company, and that company mattered.

The human twist

Humans stack another layer on top: culture. We tell stories, teach skills, and invent kitchens. Fungal chemistry still crosses our path—think edible mushrooms, molds in food storage, fermented staples, and yes, psychoactive species. These can influence states and shape learning (sometimes for better, sometimes not), but they are inputs, not blueprints.

A cultural aside often raised here is the “stoned ape” idea: the suggestion that psychoactive fungi nudged hominin cognition. In this book we treat it as an analogy for chemical ecologies shaping behavior, not as a foundation. The mechanism we’ve argued for is more basic and older: long-term cohabitation with fungal worlds training nervous systems via receptors, neuromodulators, metabolism, and plasticity. That story stands whether or not particular human traditions come into it.

What would we expect to see in bigger brains?

If this influence model holds water, then as nervous systems scale up we should notice:

• Sharper sensing where fungal cues matter. Species living in fungus-heavy habitats should be unusually good at reading those chemical landscapes.
• State tuning that fits the neighborhood. Populations exposed to reliable fungal food sources may bias toward exploration; populations facing tricky fungal hazards may prime caution and fast switching.
• Efficiency gains, not just neuron counts. Smarter behavior from better settings, not merely bigger hardware—especially in species that regularly interact with fungi.

What we shouldn’t claim

• No secret fungal “gene island” hiding in human cortex code (if it were there, we’d likely have found it by now).
• No single mushroom as the spark of human intelligence. Brains are ecosystems of causes: energy, social life, tool use, language—all layered atop the ancient network logic life discovered long before us.

Bottom line: Vertebrates, including humans, inherited the same starter kit as fungi and nematodes. We built different machines with it. But we built them in the same neighborhood, and neighborhoods leave their mark. That’s the scale-up: from conduit-based mycelial craft to animals that plan, remember, and cooperate—still running on the same three moves, just on a larger stage.

9. Counterarguments, caveats, and how this could be wrong

Good stories are fun. Breakable stories are useful. Here’s how to kick the tires on ours.

Common objections (and honest answers)

“You’re smuggling in ancestry through the back door.”
We’re not. We’ve been explicit: a fungal origin of neurons is unlikely on current genetics. Our claim is influence, not inheritance.

“Deep homology of parts can look like transfer.”
Exactly. That’s why we avoid saying fungi “gave” animals anything. Shared eukaryotic parts explain the parallels; the high-level architecture was assembled separately.

“You’re romanticizing mycelium with talk of ‘computation.’”
“Conduit-based computation” is a metaphor for a real pattern: directional growth, targeted delivery, local integration. It’s not a claim that fungi think; it’s a way to compare control logic across life.

“What about other drivers of intelligence—predation, sociality, diet?”
They matter a lot. Our point is that a fungal neighborhood can add pressure and opportunity on top of those drivers, especially early on and in small animals.

“The ‘stoned ape’ stuff?”
A cultural aside, not a pillar. We’re focused on everyday chemical ecologies over evolutionary time, not one-off altered states in hominins.

“Lab results won’t match the wild.”
Fair. That’s why we pair controlled microcosms with field microcosms and population comparisons. If the effect is real, it should appear somewhere across that gradient.

Where the hypothesis could fail

• No learning boost under real risk. If predator fungi don’t speed up avoidance learning—after careful controls—our “danger sharpens minds” claim weakens.
• No receptor change with long exposure. If lines raised for many generations in fungus-rich worlds show no shift in sensing or behavior, the influence story shrinks.
• No heritable nudge. If multi-generation exposure leaves zero trace in grand-offspring behavior (after ruling out lab artifacts), the long-game argument loses steam.
• Macro-nulls. If species that live deep in fungal neighborhoods aren’t any better at reading fungal cues than those that don’t, the ecological case goes soft.

Places we must tread carefully

• Timescales are fuzzy. “Hundreds of millions of years before bilaterians” is safer than hard dates unless we’re ready with citations.
• Teleology is a trap. Fungi didn’t “want” smarter animals. Selection just rewards whatever works in a shared neighborhood.
• Tiny effects add up slowly. We’re talking small nudges—sensing, states, plasticity—that ratchet over time. Expect modest effect sizes in any single experiment.
• Heritability ≠ new genes. Trans-generational shifts can be regulatory and fragile. We avoid over-claiming “epigenetics” unless it’s shown.

What would seriously change our mind

• A verified fungal gene island embedded near animal neural loci, replicated across methods.
• A core dendritic regulator in animals that consistently resolves inside a fungal clade on well-behaved trees (and not explained by hidden paralogs or artifacts).
• Repeated, well-powered exposure studies showing no learning/state/sensing effects despite strong fungal contact.

What would strengthen the story without hand-waving

• Long-term lines where worms reared in defined fungal “soundtracks” show faster orientation, cleaner state-switching, and a small inherited edge.
• Receptor-panel work demonstrating binding bias to common fungal volatiles in fungus-exposed lines versus controls.
• Field microcosms where mixed worm–fungus “towns” yield thriftier foraging (same calories, fewer risks/steps).

How to read negative results

A single null won’t kill a broad idea. A pattern of nulls, across sensing, states, plasticity, and heritability, should. If that pattern shows up, we’ll say so and move on—the honest outcome is that fungi were scenery, not shapers.

Bottom line: This chapter invites testing, not belief. If fungi helped animals get smarter, the footprint should be visible in behavioral shortcuts and tiny heritable nudges, especially in creatures that literally grow up inside fungal worlds. If it isn’t, we’ll write that down too.

1.10 Take-home

Fungi didn’t hand animals a brain. They handed us a neighborhood.
Living side-by-side with mycelial worlds rewarded creatures that sensed a little sharper, switched states a little faster, and learned a little better. Over time, those small wins add up. The shared eukaryotic toolkit gave both fungi and animals the same parts; similar pressures pushed them toward similar operational logics—grow toward value, route resources where they count, and integrate local signals so the next move improves. That story fits today’s genetics (no hidden merger required) and gives us experiments anyone can picture: scent mazes, predator lines, long-term exposure, thriftier foraging. Influence, not inheritance. Neighborhood, not myth. That’s how a tiny nervous system starts to look smart.

1.11 Where we go next

We’ve stayed small on purpose: mycelial webs and 302-neuron worms. Next, we scale the same three moves. Chapter 2 follows the upgrades—more sensors, richer state control, longer memories—as nervous systems climb from worms to vertebrates. We’ll ask how microbiomes (including fungi) keep tuning behavior inside larger bodies, why energy economics pays for smarter circuits, and how social life stacks onto this base to produce planning, cooperation, and culture. Different stage, same playbook—now with room for surprises.

Brains didn’t appear out of nowhere; they grew up in a fungal neighborhood—and they learned the rules.