Woman in a black and white striped singlet stands in front of a teal background holding an image of an inflamed intestine.

Dr Sarah Holper explains the science behind dreaded diarrhoea.

Diarrhoea; it’s hard to spell and equally hard to endure.

Bristol, in England’s south-west corner, is known for its suspension bridge and ‘irrepressible creative spirit’, according to its gushing tourism website. But in medical circles, the city is also known for its stool chart.

When I was an intern working on a gastroenterology ward, the Bristol Stool Chart, a seven-point scale to describe the consistency of human faeces, was provided to me as a laminated card. Type 1 is ‘separate hard lumps’; type 4 is the Goldilocks ‘smooth soft sausage or snake’; type 7 is ‘liquid consistency with no solid pieces’  – diarrhoea.

Pictured is the Bristol Stool Chart, a seven-point scale to describe the consistency of human faeces.
What does your poo stay about you? The Bristol Stool Chart is a seven-point scale to describe the consistency of human faeces.


The food you eat takes a long and winding route through your guts before it emerges from your anus as a 50-gram, soybean-paste-like cylinder. If things go wrong along that journey – through your small, then large intestine – diarrhoea can result.

The small intestine is ‘small’ in the same way Turkish delight is ‘delightful’: it’s not. It’s actually six metres long with a surface area equivalent to two car parking spaces. The ‘small’ refers to its three-centimetre calibre, compared to the wider six-centimetre ‘large’ bowel. (On semantics: ‘bowel’ covers the entirety of the small and large intestine, but ‘colon’ applies only to the large intestine.) Intestines, small or large, are muscular tubes with an absorbent lining. Their job is to suck out the nutrients from everything you swallow, propelling the dregs along and absorbing water until a 250-gram Bristol Stool Chart type 4 specimen is ready for evacuation. 

The time it takes for a bite of food to pass between your facial cheeks and your buttock cheeks varies wildly. The stomach takes two to five hours to empty. Another two to six hours elapse before the small intestine squeezes out its contents. Finally, the large intestine enjoys a leisurely 10 to 60 hours of stool contact before final evacuation. This prolonged exposure to potential carcinogens in your food is one reason why large intestine cancers are so much more common than small intestinal ones. A normal range for total gut transit is anything from 24 to 72 hours.

Your small intestine has such a ludicrously large surface area because its walls are lined with finger-like projections called villi. You’ve got 10 to 40 villi per square millimetre of small intestine. These densely packed extensions, each 0.5 to 1 millimetre long, give your intestinal wall a luxurious, velvety appearance. Each villus is in turn covered in its own microscopic villi, adding even more surface area.

To be absorbed, nutrients in your food must physically touch your small intestine’s lining. A greater surface area means a greater chance that all the chemical nutrients in your food will be absorbed. After six metres of sucking up, a watery slurry of indigestible filler material – like plant fibres, sloughed off dead intestinal wall cells, and corn kernels – remains, ready to splash into the large intestine.

The transition point from your small to your large intestine is at the lower right-hand corner of your abdomen. If you’ve had your appendix out, this is where the scar will be: your appendix dangles off your large intestine just after the small-to-large intestine juncture. Stools back up at the end of your large intestine if you’re constipated.

Your large intestine’s primary responsibility is to absorb water from the small intestine’s dregs until a solid stool is formed. Normally your large intestine absorbs 99 percent of the water you consume. And by ‘water’ I mean any liquid including coffee, milk, beer and wine (after all, once the dissolved sugar, colourings, alcohol and caffeine are absorbed, it’s just water that’s left).

Let’s imagine that you have been forced to drink one litre of sarsaparilla (I assume nobody would voluntarily drink it) – only 10 millilitres of sarsaparilla ‘water’ will end up in your faeces. Your large intestine will absorb the other 990 millilitres directly into your bloodstream. Cells in various organs will suck up whatever water they need as blood flows past them, then your kidneys will eliminate any excess water as urine. Diarrhoea happens if your large intestine fails to absorb the usual 99 percent of water from your faeces.

The word diarrhoea literally means ‘through flow’ – from the Greek dia (through) and rhoia (flow). Three main problems result in through flow: undigested food making its way to your large intestine, damage to your intestinal lining and acceleration of your intestinal squeezing rate.

Undigested food

Undigested food in your large intestine sucks in water via a process called osmosis. (Remember, all digestion should be complete once food hits your large intestine: it’s just the water absorption that’s left.) The extra water load overwhelms your large intestine’s reabsorption abilities, resulting in diarrhoea. But why would undigested food make it to your large intestine? Well, either it wasn’t digestible in the first place, or something went wrong upstream in the small intestine.

Consider the indigestible stuff first. Humans simply can’t break down certain carbohydrates in plant foods referred to as fibre.Long ago in human evolution we forfeited the laborious ability to extract calories from grass when we developed the skills to cook nutrient-dense meat. Artificial sugar substitutes like saccharin are completely indigestible: after satisfying your sweet tooth, these chemicals travel through your guts without any nutrient (i.e. calorie) absorption.

In 1996, The Lancet published the mysteriously titled case study: ‘An air stewardess with puzzling diarrhoea.’ This otherwise healthy 32-year-old woman was having up to ten loose stools a day. Against all the odds the culprit was not dodgy airline food, but her habit of constantly chewing ‘sugar-free’ gum, which is loaded with the indigestible sugar sorbitol.

You need to chew enormous quantities of sorbitol-sweetened gum before diarrhoea results: our luckless stewardess was getting through 75 grams of sorbitol a day (a stick of sugar-free gum has about 1.25 grams). Presumably, because her job required fresh breath, her daily quota of 60 sticks of gum and subsequent hospital admission with diarrhoea were tax-deductible.

Other foods, particularly sugars in fruits and dairy, are digestible – but only in small quantities. Lactose is the main sugar in breastmilk (and all milk, for that matter). Humans are born with the ability to make lactase, the digestive enzyme that breaks down lactose. Since breastmilk is usually a baby’s sole source of nutrition for at least the first six months of its life, this is obviously a crucial enzyme to possess.

Up until about 20,000 years ago, most humans lost the ability to produce lactase as they grew up. This made sense at a time when breastmilk was the only milk humans drank: why waste energy as an adult making the enzyme required to digest a food that only babies ate?

This all changed when Northern Europeans embraced cow’s milk as a year-round source of handy nutrition. A genetic mutation in the population meant that some of these Europeans retained their lactase-making ability forever, not just in infancy. When crops failed, these mutants’ lactase enzymes allowed them to survive the famine by drinking cow’s milk. Any adults without the mutation  –  those who didn’t make lactase  – couldn’t digest the lactose in the cow’s milk, which passed straight through them and caused profuse diarrhoea (as anyone with lactose intolerance today will understand). Without the cow’s milk for nutrition, people who couldn’t digest lactose were more likely to starve.

In warmer equatorial destinations like Asia and Africa, non-human milk never gained much traction as a reliable source of nutrition. Unrefrigerated dairy, sitting out in the Saharan sun, doesn’t remain edible for long. As such, the ‘make lactase forever’ genetic mutation never took hold in these areas because it didn’t offer any survival advantage.

Modern rates of lactose intolerance reflect these global differences in reliance on milk for nutrition. A 2017 study published in The Lancet found very low rates of lactose intolerance among Danish (4 percent), Swedish (7 percent) and Dutch (12 percent) citizens, compared to sky-high rates of intolerance in Japan (73 percent), China (85 percent) and Ghana (100 percent). But even the Dutch might have to lay off the Edam for a while after a gut infection. Lactase is produced in the tips of your small intestinal villi. If these are damaged by a bout of gastro, you might find that you’re temporarily lactose-intolerant.*

Even if a food is digestible, it may not be digested if things go wrong upstream of the large intestine. Food entering the small intestine is met with a stream of bile from the gallbladder and a squirt of juice from the pancreas.

Each organ’s secretions contain digestive enzymes that accelerate nutrient breakdown. Bile is also an emulsifier: it helps the fat in your food dissolve in those enzyme-rich watery secretions, rather than just float on their surface. A diseased gallbladder (blocked by a stone, for example) or pancreas (like one scarred from chronic alcohol use, or previous infection) can’t secrete its enzyme-rich juices, allowing food to pass along undigested to your large intestine. Antibiotics might kill the bacteria responsible for your middle ear infection, but they also obliterate the friendly gut bacteria that help break down your food. This collateral damage means fewer bacteria remain to keep up with the usual level of food breakdown.

Like all organs, your guts need a blood supply to work. Diversion of blood flow away from the small intestine impairs food absorption, allowing undigested remnants to flow straight into your large intestine. Intense stress is a particularly effective way to deprive your intestines of blood. Adrenaline is a stress hormone that reroutes blood away from your guts towards your lungs (to pick up oxygen) and muscles (to deliver that oxygen, allowing you to flee or fight the source of stress). When your life is in danger, digestion can wait; self-preservation comes first. Adrenaline’s blood-shunting effects – plus its ability to hasten intestinal squeezing, as we will soon discover – explains why many athletes, public speakers and exam candidates suffer the additional stress of a dose of diarrhoea before their big event.

A damaged intestinal lining

Now that we’ve digested the problems with undigested food, let’s consider the second major diarrhoea culprit: a damaged intestinal lining. Diarrhoea due to intestinal infection from contaminated food is called gastroenteritis or food poisoning. Gastro-causing pathogens invade and rupture the cells that make up your intestinal lining. Burst villi in your small intestine can’t absorb nutrients (causing diarrhoea via the ‘undigested food’ mechanism again) while an obliterated large intestinal lining can’t absorb water. Bacteria like Salmonella, E. coli and Campylobacter work in this way, as do viruses like rotaviruses – typically responsible for outbreaks of kindergarten gastro – and noroviruses – the classic cause of gastro aboard cruise ships.

Inflammatory bowel disease refers to two conditions  – ulcerative colitis (UC) and Crohn’s disease  – in which a rogue immune system causes constant intestinal inflammation. The red, swollen lining can’t function, resulting in diarrhoea.

In UC, which spares the small intestine, gradual erosion of the large intestine’s lining severely affects its water-absorbing abilities. As expected, diarrhoea can be copious in UC.

Gastroenterologists use a standardised scale to classify how severe a patient’s UC flare is. Diarrhoea up to three times a day is considered a ‘mild’ flare; the ‘severe’ label is reserved for those who suffer at least six bouts of diarrhoea per day, with visible blood.

Incidentally, UC is one of the only medical conditions (another being Parkinson’s disease) where smoking is protective. Smokers are less likely to develop UC in the first place, people with UC who smoke have less severe flares than non-smokers, and if a person with UC takes up smoking, they often experience marked clinical improvement. But the litany of health risks associated with smoking, including shaving a decade off your life expectancy, definitely outweigh any benefits.

Crohn’s disease, the other inflammatory bowel disease, tends to affect women (which is unfortunate given the homophone ‘crone’ means ‘an ugly hag’). Unlike UC, which only involves the large intestine, Crohn’s disease causes inflammation throughout the small intestine too, resulting in a double-whammy diarrhoea mechanism via impaired upstream digestion too.

An accelerated intestinal squeezing rate

The third and final diarrhoea mechanism is pretty self-evident: if your intestines squeeze too quickly there won’t be enough time for adequate nutrient and water absorption. Moving food through your intestines relies on peristalsis: sequential muscular contractions along the intestines which propel your soon-to-be-stool in the desired direction. Once or twice a day your large intestine undergoes a ‘mass movement’ or ‘giant migrating contraction’ (those are legitimate medical terms, I swear). Usually triggered by eating (your intestines need to make room for the food hitting your stomach), long segments of your large intestine vigorously contract and completely empty. If you routinely defecate every morning after breakfast, your mass movement into the toilet bowl was likely the result of a mass movement in your large intestine.

Between heroic mass movements, smaller-scale gentle peristalsis keeps your intestinal contents shuffling along. Just like your heart pumps at a regular rate, so too do your intestines. A dense network of nerves laces your intestinal walls. When one of these nerves fires, the surrounding portion of intestinal muscle squeezes and the stool inside is pushed along. The nerve firing rate is determined by pacemaker cells called the ‘interstitial cells of Cajal’ which discharge like clockwork at a regular frequency: every seven seconds in your small intestine and every 20 seconds in your large intestine. The exotic name is a nod to their discoverer Santiago Ramón y Cajal (1852-1934), a fiery Spanish neuroanatomist who, at the age of 11, built a cannon and exploded his neighbour’s side gate. Similarly explosive diarrhoea can result from anything that excites Cajal’s cells.

These cells are exquisitely sensitive to chemicals including adrenaline, ethanol, caffeine and laxatives like senna and castor oil. Castor oil was used to lubricate the rotary engines of planes during World War I. After a few hours flying, the pilots’ bowels reliably turned to water due to the effects of the ingested aerosolised castor oil fumes. The extra adrenaline from the stress of being shot at by the enemy probably exacerbated matters too.

SUMMARY: Diarrhoea is the result of too much water in your faeces. Achieving that elusive Bristol Stool Chart type 4 stool requires everything you eat to be fully digested, an intact intestinal lining, and a steady intestinal squeezing rate.

* Ed’s note – as undiagnosed coeliac disease causes damage to your villi, this is why many people with coeliac disease struggle to tolerate dairy at the time of diagnosis. In most cases, after following a completely gluten-free diet the villi return to normal and dairy can happily be consumed again.

This is an edited extract from What’s Wrong with You? By Dr Sarah Holper published by Hardie Grant Books.