You probably don’t think twice about smelling a jug of milk to check if it’s gone bad. But behind that quick decision is a symphony of genes and proteins hard at work.
A research team at Leipzig University, led by genetic epidemiologist Markus Scholz, has mapped the genetics behind our sense of smell in more detail than ever before.
In a sweeping study of over 21,000 people from Germany, Italy, and the U.S., they uncovered how our DNA shapes which scents we recognize – and how strongly we react to them.
“We identified ten genetic regions associated with the ability to detect specific odors, seven of these are new discoveries,” said Scholz. His genome-wide association study tied everyday smell performance to specific DNA changes.
The team asked participants to identify twelve scents delivered by Sniffin’ Sticks and then matched the right answers to millions of single-nucleotide polymorphisms. The exercise generated a personal odor score for every volunteer.
Two hotspots sit inside clusters of olfactory receptor genes, while others highlight specific enzymes that convert a chemical whiff into an electrical signal. Together they outline the earliest steps between sniff and perception.
One key genetic change makes people nearly four times better at recognizing the smell of fish. About one in three Europeans has it, which helps explain why some people love fish while others can’t stand the smell.
Women outperform men in smell tests across cultures. The data reveal three genomic regions whose effects flip between sexes. One variant triples women’s odds of naming orange yet does nothing for men.
Sex hormone reviews link estrogen peaks to sharper sensitivity and testosterone surges to dampening effects on smell. The hormonal picture is complex, but patterns are starting to emerge.
“The findings help to explain why women perceive smells differently during their menstrual cycle or pregnancy,” said researcher Franz Förster, who helped coordinate data. His observation echoes decades of anecdotal reports from clinicians.
Anthropologists call this the embryo-protection hypothesis, arguing that a keen maternal nose guards the fetus – though evidence remains mixed. Human genetics is starting to test that evolutionary idea directly.
Each scent in the test was linked to a different part of our DNA. Cinnamon was tied to a gene that helps detect its main ingredient, while pineapple was connected to two separate spots in the genome.
Researchers confirmed that removing an odor from the total score erased its associated signal, proving that each variant’s effect is narrow. That safeguard against statistical noise strengthens confidence in each hit.
Your pineapple gene does not help you with peppermint. That precision matters for designing clinical smell tests.
Lemon and orange were linked to smaller genetic effects, found near genes that help send smell signals, not detect them. This suggests that how the signal is processed might matter just as much as how it’s first picked up.
Smell loss is among the earliest red flags for Alzheimer’s disease. Using Mendelian randomization, the team found that high genetic risk for Alzheimer’s lowers odor-identification scores, but poor smell does not raise dementia risk.
The strongest link pointed to a gene involved in moving materials inside cells, one that’s often found alongside a known Alzheimer’s risk gene. This connection brings cell health into the picture when studying how smell and memory might be related.
Community studies linking odor discrimination to later cognitive decline back the idea that brain change erodes smell, not the reverse. Genetic data now reinforce that timeline.
Large prevention trials are now considering smell testing as a low-cost enrollment screen. Ease of administration makes the scratch-and-sniff format appealing in primary care.
Bioinformatic scans found more than forty androgen-response motifs near the sex-biased variants, far outnumbering estrogen motifs. This density hints at direct regulation by testosterone.
Yet genome-level screens showed no direct causal trail from circulating testosterone, bioavailable testosterone, or sex-hormone-binding globulin to smell scores. The null result surprised some observers.
Larger cohorts may be needed to uncover subtle endocrine effects that small studies miss. Endocrinologists are watching the space closely.
Lab teams are already planning CRISPR edits in cultured olfactory neurons to watch how these motifs alter gene output. Results from those experiments will clarify whether the motifs truly gate hormone effects.
A 200,000-participant follow-up inside Germany’s NAKO cohort is already underway and should expose weaker or rarer variants. The added power should uncover variants with much smaller effects.
Similar projects planned in East Asia and Africa will test whether diet or environment shifts genetic influence on smell. That diversity will reveal whether smell genetics follows food habits or remains universal.
Clinically, smell genotyping could tailor occupational screening for firefighters or chemical workers with innate disadvantages. Regulators already require smell tests for certain high-risk jobs.
In consumer spheres, recipe apps or fragrance firms might one day suggest products that match a user’s genetic sensitivity. Industry watchers predict fragrance personalization within a decade.
Smell genes are not part of medical care yet, but they could soon appear in direct-to-consumer DNA reports.
Ancestry services already flag lactose intolerance, and a future module may tell you that a low-sensitivity pineapple allele runs in the family. Armed with that knowledge, perfumers could tailor product lines to match regional genetic profiles.
Genes never fully dictate how we perceive aromas, but mapping their influence moves the sense of smell from mystery toward measurement.
The study is published in the journal Nature Communications.
—–
Like what you read? Subscribe to our newsletter for engaging articles, exclusive content, and the latest updates.
Check us out on EarthSnap, a free app brought to you by Eric Ralls and Earth.com.
—–