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Monday, 31 August 2026

31 Aug · Mind & body · In brief

Mind & body · Monday, 31 August 2026

Mind & body, in brief

41 stories · 57 sources

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What is moving · 1 of 4

The textbook under strain

Building ↑

two Cell papers overturned the zone map, and a 2025 study found tightly tuned receptors [2][3][1]

What is moving · 2 of 4

Smell tests pushed as an early warning

Building ↑

Parkinson's risk screens run in 1,472 and in 1,044 people [26][27]

What is moving · 3 of 4

The gap between testing and treating

High →

screens have run in over 2,500 people while the main treatment is still sniffing four scents [26][27][24]

What is moving · 4 of 4

Smell missing from health policy

High →

no country's public health agenda covers it, though about 22% of people are affected [12]

You have about 400 kinds of smell receptor, and not one of them is the coffee one

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Smell starts in a patch of tissue in the roof of your nose.

Human DNA carries 391 working smell receptor genes, and that is the whole toolkit. [1]

the same people name over 90% of familiar objects by sight [6]

Who is involved

Who is involved

Why it matters

Watch whether the tightly tuned receptors found in 2025 turn out to be the exception or the rule; if many receptors are that specific, the map from molecule to smell gets far easier to build. [1][5]

How it works

The answer is in the pattern, not in any of the parts

How it works

When you cannot have one detector for every thing, you read many rough ones at once - and then nothing inside the system holds the answer by itself.

How it works · step 1 of 5

Too many things to detect, too few parts to detect them with

How it works · step 2 of 5

So each part is made blunt: it answers to many things, roughly

How it works · step 3 of 5

Each thing then switches on its own particular set of parts

How it works · step 4 of 5

The set is the identity - the pattern is the answer, not the part

How it works · step 5 of 5

Which means no part of the system holds a label for anything

The twist

You can know a smell the instant you meet it and be unable to say what it is, because the identity was never stored anywhere as a name - only as which parts lit up.

The catch

It breaks wherever one thing matters enough to get a part of its own.

The catch

Some smell receptors are tuned tightly to a single molecule, and losing that one part costs you that one thing and nothing else.

The whole

Everyone is running a slightly different set of parts: about 60% of these genes are broken in most people, and not the same ones in each person.

The whole

Nobody gets the view from another nose, and the pairs who talk a smell through still do better than either of them alone.

Who gains

Matching single receptors to signature smells such as cork taint, grapefruit and ambergris turns odour design from trial and error into a targeting problem. [1]

Who pays

About 22% of people have some loss, and no country's public health agenda covers smell at all. [12]

Nobody knows yet

How many smells a person can actually tell apart.

Estimates have run from about 10,000 to more than a trillion. The trillion figure comes from a 2014 paper in Science and is still described in the literature as provocative. [10][11]

Nobody knows yet

Whether a smell really is a pattern across many receptors.

The textbook says yes. A 2025 study that matched human receptors to single molecules - cork taint, grapefruit, ambergris - states in its own summary that this challenges the combinatorial model. [1]

Nobody knows yet

What losing your smell means for one particular person.

An ear, nose and throat doctor at Mayo Clinic is quoted saying older adults with unnoticed total loss have a nearly 100% chance of a severe neurodegenerative disorder within five years. A clinician quoted in New Scientist puts unexplained smell loss at about one in ten going on to Parkinson's. Both cannot be right for the same person. [18][28]

Nobody knows yet

How many working smell receptors any individual has.

The reference human genome carries 391, but about 60% of the wider family is broken by mutations in most populations, and which genes are broken differs from person to person. Nobody publishes a per-person count. [1][7]

The short version

That's the story in short.

The whole story has 18 more parts.

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The whole story, in 18 parts ↓

Part 1 of 18 · Who else is involved

Part 1 of 18 · Who else is involved

Part 2 of 18 · How it unfolded

Part 3 of 18

There is no receptor for coffee.

Part 3 of 18

There is no receptor for lemon, or rain, or your grandmother's kitchen.

Part 3 of 18

Each one responds roughly, to many different molecules. [1]

Part 4 of 18

The standard account is a pattern.

Part 4 of 18

A molecule switches on some receptors and not others, and which set lights up is the smell.

Part 4 of 18

That is how a few hundred parts cover far more than a few hundred smells. [1]

Part 5 of 18

Each smell nerve cell picks exactly one receptor gene and silences all the others.

Part 5 of 18

In mice that is one out of more than 1,000, and a protein called TRIM66 does the silencing. [4]

Part 6 of 18

Every cell that picked the same receptor sends its wire to the same bundle in the smell bulb, the first stop in the brain.

Part 6 of 18

A mouse bulb holds a median of 2,851 bundles, about 2.5 for each intact receptor gene. [9]

Part 7 of 18

Camillo Golgi described those bundles in 1875.

Part 7 of 18

Nobody had counted them completely until this work; every earlier figure was an estimate. [9]

Part 8 of 18

The receptor genes themselves were found in 1991 by Linda Buck and Richard Axel, who shared the 2004 Nobel prize in medicine for it. [5]

Part 9 of 18

Two papers in the journal Cell in May 2026 redrew where the receptors sit.

Part 9 of 18

Each one occupies a set position along the roof of the mouse nose, rather than a broad zone picked at random. [2][3]

Part 10 of 18

The two maps line up.

Part 10 of 18

Where a receptor sits in the nose predicts where its wires land in the brain, through one shared set of genes. [2]

Part 11 of 18

The pattern account is under pressure from the other side too.

Part 11 of 18

In 2025 chemists found human receptors tuned tightly to single molecules: the cork taint in wine, the pepper note, grapefruit, ambergris. [1]

Part 12 of 18

One human receptor, OR52E8, answers to a single acid in armpit sweat.

Part 12 of 18

Natural variants of it respond differently from one person to the next. [54]

Part 13 of 18

About 60% of the human smell receptor gene family is broken by mutations, and not the same genes in each person. [7]

Part 14 of 18

So two people in one room are not running the same equipment.

Part 14 of 18

Where you live explains 17 to 20% of the difference in how sensitive people are to odours, measured in 1,046 people across 19 places. [16]

Part 15 of 18

What people find pleasant is more shared than that.

Part 15 of 18

In 909 people across 16 regions, region explained under 10% of the variation, and intensity varied more than pleasantness. [17]

Part 16 of 18

The pattern arrives with no name attached.

Part 16 of 18

People correctly name under half of common everyday smells, and over 90% of familiar objects they can see. [6]

Part 17 of 18

Smell takes the shortest route to feeling of any sense: only two nerve-cell junctions separate the nose from the brain's emotion circuits. [57]

Part 18 of 18

It is also the sense health systems skip.

Part 18 of 18

About 22% of people have some loss of smell and about 5% have none at all, and no country's public health plan covers it. [12][13]

Two-thirds had lost smell without knowing

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In a US study of 3,525 people, 66% of the 1,563 previously infected who reported no change in smell scored as having reduced smell on a 40-odour test, 8.2% of them severely.

Among those who did report a change, 79.8% did. [19]

Why it matters

How common smell loss is depends on whether you test people or ask them.

Who pays

Two-thirds of previously infected people who reported no change in smell scored as having reduced smell on a 40-odour test, so they are missing from every count based on asking. [19]

COVID smell loss runs for years

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A review of 21 studies covering more than 4,000 people found losses lasting from several months to over two years, with distorted and phantom smells appearing during recovery. [20]

Why it matters

The recovery is not a return to normal so much as a slow, strange rebuild.

A quarter still affected a year on

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Between 26.5% and 46% of people who had COVID still had smell loss one year after infection, falling to 8.3% at two years. [21]

Why it matters

Most people do recover, and the tail is long enough to be a public health problem.

Four bottles, twice a day, for months

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The standard treatment, olfactory training, is smelling four different scents for 10 to 20 seconds each, twice a day, for at least three months. [24]

Why it matters

It is the main thing medicine has to offer for a sense that a fifth of people have lost some of.

Who pays

The main treatment is still sniffing four scents twice a day for months, and a Mayo Clinic doctor describes half of patients as seeing no improvement after standard care. [24][18]

The sniffing works; the add-ons work harder

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A meta-analysis of eight randomised trials found training effective, with the largest gain when it was combined with the supplement PEA-luteolin, and higher recovery rates for combinations generally. [23]

Why it matters

The sniffing is the part everyone can do and the smaller part of the effect.

Nobody knows yet

How much of olfactory training is the training.

Smell also returns on its own, and the meta-analysis found its largest effects where a drug or supplement was added to the sniffing rather than in the sniffing alone. [23]

Platelet injections show a real signal

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Two 2025 meta-analyses, one of four trials in 198 people and one of seven studies in 789, found injections of the patient's own blood platelets beat placebo at 1, 3 and 12 months.

Mayo Clinic reports 87% of its patients clinically improved a year on. [21][22][18]

Why it matters

The first treatment in decades to be added to a hospital protocol for smell loss.

Who gains

Mayo Clinic reports 87% of treated patients clinically improved a year on and has added the injections to its protocol, in a field where the only other option is months of sniffing. [18]

Nasal polyps take smell first

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Between 67% and 78% of people with chronic sinus inflammation have impaired smell, and the presence of polyps is among the strongest factors. [25]

Why it matters

The commonest cause of lost smell is not a virus, it is a blocked and inflamed nose.

A five-question smell test for Parkinson's

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A shortened five-item smell test was run in 1,472 people over 60 with no Parkinson's diagnosis.

Scores fell with age, were worse in men, and tracked with a REM sleep disorder screen. [26]

Why it matters

Smell loss can precede the tremor by years, which is why a cheap test is attractive.

Who gains

Screening proposals for Parkinson's and Alzheimer's would put a test costing around $30 in front of far more people than the smell clinics currently see. [26][30][35]

Who gains

Smell offers a cheap, non-invasive marker that moves years before the tremor does, which is exactly what a prevention trial needs to recruit on. [26][28]

A quarter of over-50s screened had unexplained loss

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Of 1,044 people screened with a rapid smell test in Iran, 25% of those over 50 had smell loss with no identified cause, against under 10% of younger people. [27]

Why it matters

The screening pool is large, and most of those people will never develop Parkinson's.

Parkinson's changes which smells are pleasant

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In 94 people, only a detailed perceptual profile separated Parkinson's from other smell loss, telling the groups apart with 88% accuracy, rising to 94% when age and sex were matched.

Between 75% and 90% of people with Parkinson's have smell loss. [28]

Why it matters

The finding is not that smell fades but that the same lemon stops being enjoyable.

In Parkinson's the loss is brain-wide

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Olfactory loss in Parkinson's reflects widespread degeneration across the movement and rear cortical networks, not damage confined to the nose. [29]

Why it matters

It explains why smell tracks with later thinking problems rather than only with the nose.

Odour naming tested for early Alzheimer's

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A review of olfactory testing in mild cognitive impairment found identification and discrimination the domains most impaired in Alzheimer's, and called for tests adapted to different cultures. [30]

Why it matters

A test built around Western smells fails everywhere else, and most such tests are.

Poor smell tracked heart disease, then stopped

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In 5,142 older US adults followed 9.6 years, poor smell carried about twice the risk of coronary heart disease at year two, falling to no measurable difference by year 9.6. [31]

Why it matters

A signal that decays like that usually means something already under way, not a cause.

Nobody knows yet

Why poor smell tracked heart disease and then stopped.

In 5,142 older US adults the risk ratio was 2.06 at two years and 1.08 by 9.6 years. No mechanism is named, and a signal that fades like that is hard to read. [31]

Children's smell disorders go unlooked for

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Smell disorders affect about 22% of people overall, but only about 2% of patients at specialist smell clinics are under 18. Age-specific normal ranges for children's tests barely exist. [32]

Why it matters

A child who cannot smell gas or spoiled food has the same safety problem as an adult.

Who pays

Only about 2% of specialist smell clinic patients are under 18, and age-specific normal ranges for the tests barely exist. [32]

Cage fighters scored lower on smell

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Fourteen mixed martial arts fighters scored lower than 14 matched controls on the 40-item smell identification test, a statistically significant gap, with no difference in taste. [33]

Why it matters

The nerve fibres running to the brain pass through a thin plate of bone, and a blow shears them.

Smell identification fell after menopause

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In 80 women, those between six and ten years past menopause were far less likely to score well on odour identification than women of reproductive age. [34]

Why it matters

One of the few studies looking at smell against a hormonal timeline rather than age alone.

A questionnaire as a cheap screen

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In 228 adults, 58.3% of those over 50 had reduced smell against 19.8% of the younger group. A questionnaire correlated with formal testing, which costs around $30 a go. [35]

Why it matters

The gap between what testing costs and what a clinic will pay is why nobody is tested.

An immune signal ages the nose

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In mice, the inflammatory signal IL-17a builds up in ageing smell tissue and blocks its renewal. Blocking IL-17a restored nerve cell regeneration and reversed the tissue change. [36]

Why it matters

It reframes age-related smell loss as inflammation rather than simple wear.

A virus can leave bone behind

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In mice, a virus destroyed the smell lining, immune cells moved in and stayed, and bone formed where sensory tissue had been. The smell loss was long-term. [37]

Why it matters

A tissue that normally rebuilds itself can be replaced by something that cannot smell.

Mucus glands become emergency stem cells

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Glands beneath the smell lining that normally only produce mucus were shown to generate replacement support cells, but only after severe damage. [38]

Why it matters

A reserve nobody knew was there, held back until the usual repair route fails.

Good news

The lining inside your nose is one of the few parts of the nervous system that keeps making new nerve cells for your whole life. After severe damage, glands beneath it that normally only produce mucus start generating replacement cells too.

Some stem cells sit poised

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Single-cell profiling of olfactory stem cells found a resting group already primed for activation, with the genetic switches open around genes not yet switched on. [39]

Why it matters

It shows the tissue keeps a set of cells ready rather than starting from scratch.

Immature nerve cells do their own job

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Silencing the immature smell neurons in healthy mice impaired their ability to detect an odour, but not their ability to tell two odours apart. [40]

Why it matters

The half-built cells were assumed to be spare parts; they are a separate input stream.

The nose's bacteria are in the story

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A review links shifts in the nasal microbiome to chronic sinusitis, allergic rhinitis and post-viral smell loss, while stating the evidence is largely indirect. [41]

Why it matters

A live hypothesis that has not yet shown which way the arrow points.

Nobody knows yet

Whether the bacteria in the nose affect smell or merely travel with it.

The review states the evidence is largely indirect and does not establish which way the arrow points. [41]

What makes a scent unlock a memory

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In 106 people, 77% recognised an odour they had met one to three days earlier, and 55% of those recognitions brought back the episode attached to it.

Emotional strength predicted recognition best. [42]

Why it matters

Recognising a smell and remembering what it belongs to are two separate steps.

Smell is a poor landmark

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A review of 24 studies found people worse at remembering places by smell than by sight, by a moderate margin. [43]

Why it matters

The sense that binds hardest to feeling is one of the weakest at telling you where you are.

A matching smell speeds visual search

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In 22 people, smelling lemon while hunting for a lemon among other fruit improved speed and accuracy. A mismatched smell hurt the strongest searchers most. [44]

Why it matters

The senses are not searching separately; one primes what the other is looking for.

Pleasant smells slowed breathing, music did not

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A personally pleasant smell slowed breathing, deepened it, lowered heart rate and raised heart rate variability. A personally pleasant piece of music did none of that. [45]

Why it matters

Smell is sampled by breathing, so it can reach the calming machinery that sound cannot.

Aromatherapy trials look positive and noisy

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A review of 21 studies in pregnancy found reduced nausea and anxiety.

A review of 13 studies in new and expectant mothers found smaller effects on anxiety and sleep, with study-to-study disagreement of 88.7%. [46][47]

Why it matters

Disagreement that high means the average is describing very few of the studies in it.

Who gains

Reviews reporting real if noisy benefits in pregnancy and in hospital wards are the citations the marketing rests on, and the reviews' own heterogeneity figures do not travel with them. [46][47]

Nobody knows yet

Whether aromatherapy trials measure the oil or the expectation.

You cannot hide a smell from the person being tested. One review of 13 studies reports study-to-study disagreement of 88.7% on sleep quality, which is very high. [47]

An oil blend improved memory tasks

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In 90 adults, a commercial essential oil blend and a sage control both beat no aroma on memory and executive function tasks, measured alongside blood oxygen in the brain. [48]

Why it matters

The control condition was another smell, which is the harder and rarer comparison.

Lavender's pain effect traced in mice

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Inhaled lavender oil eased migraine-like pain in mice through a specific brain circuit running from the smell region to the hypothalamus. Blocking one receptor in that circuit abolished the effect. [49]

Why it matters

A mechanism means the effect can be tested rather than only reported.

Horses read human fear odour

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Forty-three horses exposed to pads carrying human fear odour startled harder, gazed longer at novel objects and touched the person less than with joy or control pads. [50]

Why it matters

The chemical signal crosses species without either side intending to send it.

Mosquitoes pick people by chemistry

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Across 42 women, pregnancy and the phase of the menstrual cycle changed how attractive they were to yellow fever mosquitoes.

Twenty-seven volatile compounds were identified, one of them enough on its own to shift preference. [51]

Why it matters

Who gets bitten is a chemistry question, and it changes over weeks.

Fear in parents showed in offspring's noses

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Mice trained to fear an odour grew more neurons carrying the matching receptor. So did their own offspring, who had never met the odour. [52]

Why it matters

The receptor mix a nose is built with is not fixed at birth by genes alone.

First structure for a greasy-smell receptor

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A cryo-electron microscopy structure of a class II smell receptor showed an unusually large water-repelling pocket for fatty acid molecules and an unconventional way of switching on. [53]

Why it matters

Smell receptors have been almost unphotographable, which is why so few are matched to smells.

Two noses beat the better one

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Pairs of people who discussed a smell and agreed a joint answer outperformed the better of the two individuals, on both discrimination and identification. [10]

Why it matters

Words fail for smell, and talking still helped, which nobody expected.

How perfume gets described in Chinese

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An analysis of 29,372 reviews of 36 perfumes found descriptions leaning heavily on naming the source of a smell rather than on qualities of it. [55]

Why it matters

With no vocabulary for smells themselves, every language borrows the names of things.

Phantom smells have no validated test

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Phantosmia is smelling something that is not there. Reliable validated tests for these distortions of smell quality do not currently exist. [56]

Why it matters

A symptom that cannot be measured cannot be counted, treated or trialled.

Dogs carry twice the gene set

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Individual dogs carry 779 to 807 working smell receptor genes, against about 400 in humans and 1,100 in mice.

A dog's nose is reported to hold 125 to 300 million receptors, against roughly 5 million in a person. [8][14]

Why it matters

The first number is how many kinds; the second is how many copies. The gap is the size of the array, not a different kind of sense.

Mountain mammals gave up smell genes

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Across 27 mammal species living only above about 1,000 metres, the genes that had broken were heavily concentrated in smell receptors: about 23% fewer of them, and smell bulbs about 18% smaller than in lowland relatives. [15]

Why it matters

Thin air carries fewer odour molecules, and unused genes are not maintained.

Hunter-gatherers kept more of the set

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Genomes from 50 Indigenous people of the Malay Peninsula showed fewer broken smell receptor genes than other populations.

One farming group carried a distinct version of OR12D3, a gene also linked to insulin release. [7]

Why it matters

How people get their food appears to have shaped which smells they can still detect.

The truth, across the day

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What's really going on

Smell is being turned into a cheap early-warning test for brain disease faster than it is being understood, while the treatment for losing it is still four bottles and three months of sniffing.

Why it works on people

One enormous number does the work in each direction: a trillion smells, and a nearly 100% chance of neurodegenerative disease, are both repeated far more often than the studies underneath them.

That's the whole Mind & body day.

41 stories, 57 sources.