The Nose Knows Nothing Anymore: The Politics of Disgust

It is Popcorn or Dirty Dog Feet?

There is a molecule called nonanal.

You will not find it on any list of things you are supposed to care about. It is not glamorous. Nor is it controversial. It is a nine-carbon aldehyde, colourless and oily, produced naturally by the oxidation of lipids — a fancy way of saying it’s what happens when fats go off. It is present in rancid cooking oil, in the exhaled breath of people with certain lung cancers, and in the scent profile of aging human skin. Also, I have recently learned that it is one of the compounds that makes popcorn smell like popcorn (and also what defines the bouquet of dirty dog feet).

I mention nonanal because it sits at a crossroads. It is a molecule of warning and of pleasure, depending on context. The nose, encountering nonanal, must decide which is which. Given sufficient olfactory sophistication, it will get it right most of the time. Given a degraded or blunted olfactory system — with which, as we will discover, an alarming proportion of us are afflicted — the message may arrive garbled, or not at all.

The implications of that garbling, I have come to suspect, are considerably larger than popcorn or your dog’s smelly feet,

The Ancient Sniff-Test

Let us start, as one should, at the beginning. Or at least at the beginning of the problem.

Sometime between the emergence of our non-human primate ancestors and ourselves, humans began losing olfactory receptor genes. This is not a recent deficiency; it has been happening for millions of years, as vision became the dominant sense and the olfactory gene repertoire quietly contracted. We emerged from this evolutionary process with approximately 800 olfactory receptor genes, which sounds generous until you learn that mice have roughly twice as many, and that any two humans will differ in the function of over thirty percent of their odourant receptors. Put plainly: you and I may be smelling fundamentally different worlds without knowing it, because we have never compared notes in any meaningful way, and because the world has never given us a particularly good reason to try.

This evolutionary background hum of olfactory decline is, however, the least of our current problems. The more pressing concern is what is happening to human olfaction in real time, in the lifetimes of people currently alive, in communities that can be mapped and measured — and, in some cases, voted in elections.

The last statement seems out of place? No, it isn’t. Read on.

Somewhere between thirteen and thirty percent of older North American adults have objectively measurable olfactory dysfunction. One in ten Americans over 40 years of age report an issue with smell. By the time you reach 85, the probability of losing the ability to identify a specific odour over the next five years runs between 29 and 45 percent, depending on the odour. Men’s deteriorate faster than women, African Americans quicker than white Americans.

And… this is not a non-sequitur: Rural populations, intriguingly, use more antidepressants than urban ones — but I am getting ahead of myself.

“It Must be Something in the Water”

Why is this happening? Several reasons and they are worth enumerating because they will resurface later in ways that may surprise you.

Air pollution is the most thoroughly documented environmental culprit. Fine suspended particles of less than 2.5 microns in diameters (PM2.5), produced by vehicle exhaust, industrial emissions, and combustion of every kind, does not stay politely in the lungs. It follows the olfactory nerve directly into the brain. Studies comparing residents of Mexico City with those in less polluted rural areas found mild to severe olfactory impairment in thirty-five percent of the urban population, versus twelve percent of the rural. Autopsies on Mexico City residents found ultrafine particles physically lodged in the olfactory bulb. Johns Hopkins research found that long-term PM2.5 exposure increases the risk of smell loss by roughly sixty to seventy percent.

Beyond pollution: viral infections of the upper respiratory tract have been stripping people of smell for as long as there have been viruses, which is to say, forever. This is an infamous symptom of COVID-19, but it’s not new condition; it has merely been widely recognized. Aging reduces neurogenesis in the olfactory bulb. Head trauma disrupts olfactory circuitry. Then there are the medications, specifically, the antidepressants that approximately eleven percent of American adults and somewhere between 13 and 16 percent of Canadian adults are currently taking, with numbers that have been climbing steadily since the mid-1990s and accelerating sharply since 2020.

In Canada’s Atlantic provinces, the situation is remarkable enough to warrant its own pause. Nearly a quarter of the adult population is on antidepressants. Among women aged 25 to 44 in that region, the figure reaches 37 percent. These provinces are also among the most economically distressed regions of the country, with aging rural populations and limited mental health infrastructure outside of medication. They have, for what it is worth, also historically returned some of the most durable patterns of political conservatism in the country, though the relationship between these facts is exactly what this essay is attempting to untangle — carefully, and without undue confidence.

"Something Smells Rotten" Or “I Can't Smell A Thing”

There is a relationship between the loss of smell and mental illness that has been quietly documented for decades, and rather underappreciated until recently.

Let me be specific, because it matters. The olfactory system is neurologically unusual. It is the only sense that connects directly, largely unmediated, to the limbic system: the amygdala, which processes emotional valence; the hippocampus, which consolidates memory; and the orbitofrontal cortex, which assigns reward value to experience. No other sense has this direct access. This is why smell triggers memory and emotion with an immediacy and vividness that vision and hearing cannot match. It is also why olfactory loss does not stay neatly within the borders of the nose.

Use It, Lose It, and Never Know Why

With the loss of their sense of smell, people also lose much of the hedonic richness of daily life. Up to 70 percent report decreased pleasure in food and drink. They describe a world that has become flatter, less textured, less worth inhabiting with the same enthusiasm. The technical term for this is anhedonia, the inability to experience pleasure from activities formerly found enjoyable, and it is one of the primary diagnostic markers of clinical depression. The connection is not incidental; research has confirmed that olfactory impairment predicts the development of depression in older American adults, and that depressed patients show reduced olfactory bulb volume that correlates with the severity of their illness.

The conditions documented as consequences of smell loss are worth listing in full: depression, anxiety, social isolation, loneliness, sexual dysfunction, reduced relationship satisfaction, diminished self-confidence (specifically around fear of undetected body odour). Something that the research calls, rather dryly, “smell loss-induced anhedonia,” is distinguished from regular anhedonia by the additional cruelty that sufferers often don't realize the connection. Their world has become less pleasurable, yet they don't know why.

A great many people might be impacted. One imagines them scattered across rural communities, growing old, taking their antidepressants, not getting better quite enough, and not understanding quite why.

Enter the Antidepressants

The relationship between antidepressants and olfactory function is one of the more peculiar chapters in this story, and it goes in both directions at once, which is the sort of thing that makes it a topic genuinely interesting and difficult.

Depression, we now know, is associated with reduced neurogenesis in the olfactory bulb. The stress hormones that drive depression, particularly elevated cortisol, impair the olfactory system’s capacity to renew itself. Animal studies have shown that olfactory bulb damage induces depressive behaviour; removing the olfactory bulb in rodents is a reliable model for producing depression-like states. Conversely, antidepressants can restore neurogenesis in the olfactory bulb and thereby improve olfactory function.

So antidepressants can help. But the picture is more complicated.

So hold on, we’re going to get technical for a few paragraphs. But stay with me — it all connects…

The Chicken or the Egg?

Animal studies have also shown that both SSRIs and SNRIs — the medications most commonly prescribed — produce significant decreases in olfactory sensitivity during treatment, mediated by their alteration of serotonin and noradrenaline transmission in the olfactory bulb. Clinical case reports document specific antidepressants — sertraline, fluoxetine, paroxetine, vilazodone — inducing hyposmia or anosmia that resolved when the medication was discontinued. The mechanism proposed is the same one that makes the medications useful: they act on the neurotransmitters concentrated in the olfactory bulb, and the olfactory bulb turns out to be, in some patients, a casualty of the collateral recalibration.

Who’s on First? No, Really

The research is frank about the difficulty of disentangling this. Depressed patients show olfactory impairment. Are they impaired because they are depressed? Because they are medicated? Because the underlying neurobiology that drives their depression also drives their olfactory decline? The honest answer is that we do not fully know, because the studies that would settle the question have not, for the most part, been designed or funded.

What can be said is this: there is a cycle. Depression degrades olfactory function. Olfactory loss deepens anhedonia and social isolation, which worsen depression. Some antidepressants may further blunt olfactory sensitivity in some patients, potentially reinforcing the very impoverishment of experience that the medication was meant to address. The cycle runs — years, for many people.

Here, There be Dragons

Let me be clear: This is where this essay takes its most speculative turn. What follows is a dive into my own meandering reasoning, not established fact. It is the sort of reasoning that cannot be confirmed or refuted because no study has been designed to test it. I offer it in the way I sometimes think: I try on the clothes of an answer, to see whether it fits.

And, for the most part, despite all the medical and psychological jargon I have dragged into the matter to buttress my presentation, these speculations are mine.

That established, let us proceed.

Enter Disgust: “You’re Not Going to Drink From That Are You?”

There is a substantial and contested body of research linking disgust sensitivity — specifically, heightened aversion to contamination and interpersonal transmission of pathogens — to political conservatism. The specific disgust I mean is the kind that makes a person unwilling to share a glass of water with someone outside their immediate family; the kind that manifests as intense discomfort with anything that violates the body’s boundaries or mingles substances that should remain separate; the kind that raises the particular alarm of this is not clean, this is not safe, this is not known.

A large study covering over 31,000 participants across 121 countries found a consistent positive relationship between contamination disgust and conservative voting behaviour. Other researchers, drawing on Jonathan Haidt’s Moral Foundations Theory, have identified a “Purity/Sanctity” moral foundation — shaped by the psychology of disgust and contamination — that conservatives activate more readily than liberals, alongside their equal or greater reliance on all other moral foundations. The relationship is real, though the mechanism has been debated vigorously, and some original research claims have been qualified: liberals are not less disgusted than conservatives overall; they are disgusted by different things (tax evasion and xenophobia score high for liberals; homosexuality and bodily contamination score higher for conservatives). The general capacity for disgust does not separate the two groups. The trigger does.

Disgust is, at its evolutionary root, an olfactory-guided emotion. The smell of rot, feces, spoilage, disease: these are the original disgust stimuli, and smell is the primary detection mechanism. We wrinkle our nose; we recoil; we are kept safe from pathogens our immune system has not yet had to fight. The nose is the first-line soldier of the behavioural immune system, which is the psychologists’ term for the collection of emotional responses that evolved to keep us away from things that might infect us.

What happens with disgust when olfactory capacity degrades? When the nose stops working reliably, what happens to the system it serves?

It Does Not Go Gentle into that Dark Night

To paraphrase Dylan Thomas, I propose that our nose does not simply go quiet; a system deprived of its primary data source does not conclude there is nothing to worry about. It concludes, instead, that its data is unreliable and that the appropriate response is to raise its baseline level of threat-assumption. Unable to accurately smell whether the shared glass, the stranger, the novel food, the unfamiliar social situation carries pathogenic risk, the sensible thing, in evolutionary terms, is to treat all of them as potentially risky. The system calibrates upward in the absence of good information, because the cost of a false negative (failing to avoid an actual pathogen) is historically higher than the cost of a false positive (avoiding something harmless).

This would produce exactly the profile that characterizes heightened contamination disgust: increased wariness of outsiders; stronger preference for the known and the familiar; more rigid maintenance of social and physical boundaries; more discomfort with the sharing of bodily-adjacent objects and spaces; and more instinctive alignment with institutions and traditions that impose order on a world that feels, without exactly knowing why, less trustworthy than it used to.

It would not feel like a failure of the nose. Ironically, it would feel like common sense.

The Many Connections of Erdős

I find Paul Erdős work fascinating and have touched briefly upon his insights in a previous essay. Erdős was a Hungarian mathematician who spent his life looking for the hidden structure underlying apparently unrelated things. His great insight — borrowed from graph theory — was that when multiple independent paths converge on the same point, the convergence is not coincidental. It is evidence that you have touched something real.

I am not a mathematician, nor a scientist, and this is not a proof. But I want to shed daylight on the hidden node that three threads of this essay converge upon.

The Triangulation of a Notion

The hidden node is the olfactory-limbic valuation circuit: the neural pathway that connects olfactory input to the amygdala and orbitofrontal cortex, and that performs the fundamental calculation every nervous system must make: is this environment safe enough to explore, or threatening enough to defend against?

Thread one reaches this node through the contamination-disgust pathway: smell loss degrades the circuit’s primary input, driving it toward defensive default.

Thread two reaches it through the anhedonic pathway: smell loss strips reward signals from the circuit, shifting the approach-avoidance ratio toward avoidance, contracting the experienced world, fostering a psychology of protection over exploration.

Thread three reaches it through pharmacology: antidepressants act directly on the neurotransmitters regulating this same circuit, altering its gain without necessarily improving the quality of its sensory data, and in some patients possibly blunting the olfactory input further.

All three arrive at the same place. The circuit, assailed from three directions simultaneously, runs hotter on threat and quieter on reward. Yet, the person it belongs to does not realize that this is happening. They experience it as a conclusion rather than a symptom: the world is less trustworthy; novelty is less appealing; familiar things deserve protecting; and strangers should probably not drink from your glass.

West Virginia, Kentucky, Vermont, New Hampshire and… Atlantic Canada…?

I do not want to overstate this. The geography of antidepressant use in North America does not map cleanly onto any political topology. West Virginia and Kentucky, which are among the highest antidepressant-using states in the US, vote Republican by enormous margins. But so do rural communities across the continent, and rural communities also show the highest rates of olfactory dysfunction, the most economic distress, the most limited mental health infrastructure, and some of the highest rates of viral illness and occupational chemical exposure. Vermont, also near the top of antidepressant use, votes Democratic. New Hampshire splits. Canada’s Atlantic provinces, the highest-use region in the country, have historically leaned Liberal federally while harbouring Progressive Conservative provincial governments that are functionally quite different from the ideological conservatism measured in the disgust-politics literature.

What A Mess! It’s Complicated

The correlations are real but messy. They are made messier still by the treatment gap: conservatives, research consistently shows, are significantly less likely to seek or receive mental health treatment despite reporting equivalent rates of depression. Among those with depressive symptoms, nearly three-quarters of Republicans have unmet mental health care needs, versus just under 60 percent of Democrats. The antidepressant data therefore understates the mental health burden in more conservative communities, which means the population of people experiencing smell loss and depression without pharmaceutical intervention is proportionally larger in those communities, not smaller.

There is, I think, something genuinely uncomfortable in all of this — not politically, but societally. There is a population of people experiencing a quiet and largely invisible sensory loss that is making their world less pleasurable, more threatening, and more opaque. Some of them are medicated in ways that may compound the problem. Most of them do not know any of this is connected. The connection has not been studied, because no one has thought to design the study. The olfactory-limbic circuit, sitting at the intersection of sensation, emotion, memory, and social orientation, has been substantially ignored by the research programmes that might illuminate it.

Back to Popcorn, Rancid Butter, and Dog Feet

I began with nonanal, and I want to return to it.

There is something philosophically instructive about a molecule that can mean danger or pleasure depending on the proper functioning of the nose receiving it. In rancid fat, it warns. In popcorn, it rewards. The chemistry is identical; the context is everything; and the nose, if working correctly, knows the difference.

A compromised nose does not know the difference. Rather, it cannot be trusted to know, and so the rational response is to treat ambiguity as threat. And in a world where noses are getting less reliable, the threats are proliferating, the pills don't quite fix the underlying problem, and the popcorn still smells like popcorn to everyone else but you — though you don't know that, because you’ve never compared notes — the appropriate response may feel, from the inside, indistinguishable from wisdom.

The difficulty is that it is also indistinguishable from a slow, invisible recalibration of an entire population’s relationship to novelty, trust, and the stranger at the table.

Whether you offer them your glass or drink from theirs is, of course, your business entirely.

But the nose that informed that decision may no longer be the instrument you think it is.

Further reading for the curious: Richard Doty's work on olfactory epidemiology; Jonathan Haidt's The Righteous Mind; and the Monell Chemical Senses Center's ongoing research on olfactory decline. Not cheerful reading, but instructive.