Why Do We Hiccup? | The Everyday Biologist

Hiccups are one of the strangest things the human body does on a regular basis, mostly because nobody can agree on why it does them at all. Sneezing clears the nasal passages. Coughing clears the airway. Hiccups don’t seem to clear anything, and yet everyone experiences them, fetuses do it in the womb before they can even breathe on their own, and newborns spend a startling percentage of their time doing it. So what’s actually going on, and why hasn’t evolution gotten rid of something that looks, on the surface, completely useless?

What a hiccup actually is, mechanically

A hiccup, medically called singultus (from the Latin for “sob” or “gasp”), is a sudden, involuntary contraction of the diaphragm and the external intercostal muscles, followed about 35 milliseconds later by an abrupt closure of the glottis [4]. That timing gap matters. The muscles fire first, air starts rushing in, and then the vocal cords slam shut mid-breath, which is what produces the characteristic “hic” sound. This combination, forceful inspiratory effort plus glottal closure, is what separates a hiccup from a gasp, a sniff, or a sigh, all of which involve similar muscles but without the same abrupt vocal cord adduction [4].

The reflex runs through a three-part arc. The afferent limb carries signals in from the phrenic nerve, the vagus nerve, and the sympathetic chain (T6 to T12), picking up sensory information from the esophagus, stomach, and diaphragm [1,3]. Those signals converge on a central processing unit, thought to sit in the medulla, possibly involving the periaqueductal gray and subthalamic nuclei [1]. From there, the efferent limb sends motor commands back out through the phrenic nerve to the diaphragm and through accessory nerves to the intercostal and scalene muscles [1,3].

The neurotransmitters involved are reasonably well characterized even if the bigger picture isn’t. GABA, dopamine, and serotonin are the main players at the central level, while epinephrine, norepinephrine, acetylcholine, and histamine act peripherally [1]. This is why such a wide range of unrelated drugs, baclofen, chlorpromazine, gabapentin, and even SSRIs, can all interrupt intractable hiccups. They’re hitting the same reflex arc from different angles, not treating a single underlying cause [1,3].

Hiccups start absurdly early

One detail that any theory of hiccups has to account for is timing. Hiccups have been documented by ultrasound in the human fetus as early as 10 weeks of gestation, which is before either breathing movements or swallowing sequences appear [5]. They continue through the second and third trimesters, often occurring in regular runs that can happen independently of fetal breathing movements or alongside them [3,5]. Newborns hiccup constantly, by some estimates up to 2.5% of their waking time, and the frequency then drops off through infancy, leaving only occasional short bouts for the rest of life [2].

This developmental pattern is a big part of why researchers keep circling back to the idea that hiccups aren’t a random glitch. A reflex that shows up this early, this consistently, and this far ahead of other motor behaviors looks like it’s doing something, even if that something isn’t obvious once you’re an adult who no longer needs it, or needs it much less.

Three competing theories, none of them settled

The burping hypothesis. Daniel Howes proposed that hiccups evolved to clear swallowed air from the stomachs of nursing infants [2]. The logic starts from the sharp drop in intrathoracic pressure that a hiccup produces. Of the possible things that pressure drop could move (blood, lymph, air in the trachea, or material in the esophagus), Howes argues the esophagus is the only one that fits both the anatomy of the afferent nerves and the direction of the pressure change. An air bubble sitting in the stomach or lower esophagus could trigger the reflex, and the resulting pressure drop would pull that air up into the mid-esophagus, where it could then be expelled on the next exhale [2]. Since infants who nurse continuously are especially prone to swallowing air along with milk, and since more stomach capacity for milk means better nutrition, a reflex that clears that air would offer a real survival advantage, and would explain why hiccups are so much more common in infancy than at any later point in life [2]. Nobody has proven this. Howes himself frames it as a hypothesis in need of testing, not a conclusion.

The bolus-clearing theory. An older and related idea is that hiccups exist to dislodge food trapped in the esophagus. It has some support from the fact that the afferent nerves involved do pick up signals from the lower esophagus, and it would explain the relaxation of the lower esophageal sphincter that accompanies a hiccup [2]. But it runs into a problem: a hiccup would push a stuck food bolus toward the middle of the chest, away from the stomach where it could actually be digested and toward the airway, where it becomes more dangerous, not less [2]. It also doesn’t explain why hiccups are so common in newborns who aren’t eating solid food at all.

The phylogenetic relic theory. Straus and colleagues took an entirely different angle, arguing that hiccups aren’t adaptive at all in the modern sense, but are instead leftover machinery from how our aquatic ancestors breathed [4]. Before lungs, and before the diaphragm even evolved, early air-breathing vertebrates used buccal muscles to pump water over their gills while keeping the glottis closed to prevent flooding the lung, a motor pattern still visible in tadpoles and other amphibians [4]. Straus argues that hiccups share a striking number of properties with this ancestral gill-ventilation pattern: both involve a central pattern generator in the brainstem, both close the glottis during inspiration, both are suppressed by higher carbon dioxide levels, and both can be shut down by baclofen at surprisingly similar doses [4]. Under this model, hiccups aren’t a burping reflex or a bolus-clearing reflex with a job to do. They’re a fragment of an ancient breathing circuit that never fully disappeared, possibly because parts of that same circuit got repurposed for something still useful, like suckling [4].

None of these three theories has been demonstrated conclusively, and they aren’t mutually exclusive. It’s entirely possible that an ancestral gill-ventilation circuit (Straus’s explanation for where the wiring came from) got co-opted for a burping function in infancy (Howes’s explanation for why it’s still around), and just never got switched off completely in adults.

Why hiccups sometimes won’t stop

Most hiccup bouts resolve on their own within minutes and are triggered by fairly mundane things: eating too fast, carbonated drinks, sudden excitement, gastric distension [1,3]. Classification runs on duration. An acute bout lasts under 48 hours. Persistent hiccups last more than 2 days, and intractable hiccups continue past a month [1,3]. Persistent and intractable cases are the ones worth paying attention to, since they’re associated with an actual pathological process affecting the reflex arc somewhere along its length, ranging from GERD and hiatal hernia to brainstem lesions, mediastinal tumors, and stroke [1,3].

There are roughly 4,000 hospital admissions for hiccups every year in the United States, and intractable hiccups are far more common in men (82%) than women, most of them over 50 [1]. Left untreated, chronic hiccups can wreck someone’s quality of life, causing exhaustion, weight loss, and depression [3]. Treatment tends to work by either dialing down the input from the gastrointestinal tract to the hiccup center or by directly suppressing the excitability of the central pattern generator itself, which is why drugs targeting GABA, dopamine, and serotonin all show up as viable options despite having almost nothing else in common [1,3].

Summary

The mechanics of a hiccup are well understood: a coordinated burst from the diaphragm and intercostal muscles, glottal closure 35 milliseconds later, orchestrated by a brainstem pattern generator and modulated by GABA, dopamine, and serotonin. What that mechanism is actually for is still an open question. It might be an infant burping reflex, a leftover fragment of how fish-like ancestors ventilated their gills, or some combination of the two that got tangled up with the evolution of suckling. What’s clear is that hiccups show up too early in development and too consistently across mammals to be dismissed as pure noise, even if science hasn’t landed on a single answer for why they’re there.

Common Questions

Why do hiccups happen more in babies than adults?

Newborns spend as much as 2.5% of their time hiccupping, and the reflex is active in the fetus from around 10 weeks gestation, well before breathing or swallowing patterns appear. It then drops off sharply through infancy, with only occasional short bouts for the rest of life.

Is there an agreed-upon reason we hiccup?

No. There's a well-mapped reflex arc that explains how a hiccup happens, but why the reflex exists at all is still unresolved. Several competing hypotheses exist, and none has been proven.

What actually causes a hiccup at the neurological level?

A putative pattern generator in the brainstem triggers a sudden, coordinated contraction of the diaphragm and intercostal muscles, followed about 35 milliseconds later by an abrupt closure of the glottis. GABA, dopamine, and serotonin are the central neurotransmitters most consistently implicated.

Can hiccups be a sign of something serious?

Usually not. Most bouts resolve within minutes. But hiccups lasting more than 48 hours are classified as persistent, and those lasting more than a month are classified as intractable, both of which are more likely to point to an underlying condition affecting the reflex arc, from GERD to brainstem lesions.

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