Appearance
9.6 — The Large Intestine and the Microbiome
The large intestine receives about 1.5 litres of liquid waste a day and returns about 100 to 200 ml of it as stool. It absorbs almost no nutrients directly. Its main resident population — roughly 38 trillion bacteria — does more chemistry for you than the organ itself does, and they collectively carry perhaps 150 times more genes than your own genome.
This chapter is about both, and about being honest where the science is strong and where it is being oversold.
The structure
About 1.5 metres long and wider than the small intestine — hence the name, which refers to diameter rather than length.
Caecum — the pouch where the small intestine empties in, in the right lower abdomen. The appendix hangs from it.
Ascending colon — up the right side. Transverse colon — across. Descending colon — down the left side. Sigmoid colon — the S-shaped segment in the left lower abdomen. Rectum — the final 12 to 15 centimetres. Anal canal — about 4 centimetres.
Three features distinguish colon from small intestine. The longitudinal muscle is gathered into three bands rather than forming a complete layer; those bands are shorter than the colon so they pucker it into pouches; and there are small fat-filled tags on the surface. The pouching is what makes a colon recognisable on any scan or X-ray.
There are no villi. The colon is not built for nutrient absorption.
The ileocaecal valve guards the entry and prevents colonic contents refluxing back into the small intestine, where bacteria would overgrow.
What it does
Absorbs water and electrolytes. Sodium is pumped out actively and water follows.
And the reserve capacity is large — the colon can absorb up to about 5 litres a day if needed. This is why small intestinal disease does not necessarily cause diarrhoea: the colon compensates. Diarrhoea from a small intestinal cause means the colon's capacity has been exceeded.
Absorbs vitamins made by bacteria — vitamin K, biotin, and several B vitamins.
Ferments what your enzymes could not digest — dietary fibre and resistant starch.
Stores and eliminates waste.
Transit time through the colon is 12 to 48 hours, against 3 to 5 hours through the small intestine. Most of the time food spends in you is spent here.
The microbiome
Roughly 38 trillion bacterial cells, mostly in the colon, weighing around 200 grams in total (Chapter 1.1). The old claim that they outnumber your cells ten to one is wrong; the ratio is close to one to one.
Several hundred to a thousand species per person, dominated by two groups, with the composition varying enormously between individuals. Two healthy people may share only a minority of their species, which is one reason it has been hard to define a "healthy" microbiome.
What is well established:
They ferment fibre into short-chain fatty acids — mainly butyrate, propionate and acetate. Butyrate is the primary fuel for the cells lining your colon, which is a striking arrangement: those cells feed on a bacterial waste product rather than on nutrients from the blood. This is a genuine mutual dependency, and it is the strongest single argument for eating fibre.
They synthesise vitamins — vitamin K and several B vitamins, contributing a meaningful fraction of daily needs.
They occupy the space — colonisation resistance. A dense established population makes it hard for a pathogen to gain a foothold, and this is why antibiotic-associated infection happens.
They train the immune system. Germ-free animals have poorly developed gut immune tissue and abnormal immune responses. Around 70 percent of your immune tissue is in the gut, and much of its development depends on bacterial exposure.
They metabolise drugs. Some medicines are activated or inactivated by gut bacteria, and this contributes to differences in response between people.
What is plausible but not settled:
Links to obesity, diabetes, inflammatory bowel disease, allergy, autoimmunity, mood and behaviour. The associations are real and reproducible. Causation, and direction of causation, is much less clear, and animal studies frequently do not transfer to humans.
The "gut–brain axis" is a real anatomical and chemical connection — the vagus nerve, immune signalling, and bacterial metabolites that affect the brain. The specific claims made in popular writing about mood and behaviour run well ahead of the human evidence, and it is worth being sceptical of any product sold on that basis.
What is not supported:
That there is one correct microbiome to aim for. There is not; healthy people vary hugely.
That most commercial probiotics reshape your microbiome. Most transit through without establishing. Specific strains have specific evidence for specific conditions — certain strains reduce antibiotic-associated diarrhoea, and certain strains reduce necrotising enterocolitis in preterm infants — but "probiotic" as a general category is a marketing term, not a treatment.
That microbiome tests sold direct to consumers are clinically useful. They are not, currently. The variation between healthy people is larger than the differences the tests claim to interpret.
What actually shapes your microbiome: diet, and especially fibre diversity — the number of different plant foods eaten, more than the total quantity; antibiotics; mode of birth and early feeding; age; and geography. Diet changes it within days, which is encouraging, and the change reverses just as fast when the diet reverts.
When it is disrupted
Clostridioides difficile infection is the clearest case of a microbiome disaster with a clear cause and a remarkable cure.
Antibiotics wipe out the normal population. C. difficile, which is resistant and may be present in small numbers or acquired from the environment, expands into the empty space and produces toxins. The result is severe diarrhoea, colitis, and in severe cases a massively dilated colon that can perforate.
Treatment is a targeted antibiotic — and about 20 to 25 percent relapse, because the antibiotic also prevents the normal population re-establishing.
Faecal microbiota transplantation is the striking part. Stool from a screened healthy donor is transferred into the patient's gut, restoring a normal population. Cure rates for recurrent C. difficile are around 85 to 90 percent, considerably better than antibiotics, and this is one of the best-evidenced interventions in the whole microbiome field.
It works well for this one indication. Claims that it treats obesity, autism, depression or autoimmune disease are not currently supported by adequate trials, and doing it outside a clinical setting is genuinely dangerous — transmissible infections have been passed this way.
The appendix
A narrow blind-ended tube 5 to 10 centimetres long hanging from the caecum.
For a century it was described as vestigial and useless. The current understanding is more interesting: it appears to act as a reservoir of gut bacteria, a protected side-pocket from which the colon can be recolonised after an episode of severe diarrhoea has flushed it out. It is also rich in lymphoid tissue.
People with an appendix recover their normal flora after C. difficile infection more reliably than those without, which supports the reservoir idea.
Appendicitis affects around 7 to 8 percent of people at some point. The mechanism is blockage of its narrow opening — by a hardened lump of stool, lymphoid swelling, or rarely a tumour. Bacteria multiply in the closed space, pressure rises, the blood supply is compromised, and it perforates.
The classic presentation and why the pain moves was explained in Chapter 4.1: central vague pain first, shifting to the right lower abdomen over hours as the inflammation reaches the parietal peritoneum. Then anorexia — which is so consistent that a person with a normal appetite rarely has appendicitis — nausea, low-grade fever, and localised tenderness.
Presentation is often atypical, particularly in children, the elderly, and pregnancy, where the enlarging uterus displaces the appendix upward.
Treatment is usually appendicectomy, now almost always laparoscopic. Antibiotics alone cure a substantial proportion of uncomplicated cases, and this has become a genuine option — around 60 to 70 percent avoid surgery at one year, with the rest eventually needing it. It is a reasonable choice for some patients and a real change from the previous absolute rule.
Defecation
Mass movements — strong contractions sweeping the colon — occur one to three times a day, typically after meals. This is the gastrocolic reflex, and it is why people often need the toilet after breakfast.
When stool enters the rectum, stretch receptors trigger the urge.
Two sphincters, and the arrangement is what makes continence possible.
The internal anal sphincter is smooth muscle, involuntary, and relaxes automatically when the rectum fills.
The external anal sphincter is skeletal muscle, under voluntary control.
So the internal one opens automatically and the external one is what you hold shut. If it is not convenient, voluntary contraction of the external sphincter and the pelvic floor pushes the stool back, the rectum relaxes, and the urge subsides for a while.
And there is a piece of anatomy that changes how easily it works. The puborectalis muscle slings around the junction of rectum and anal canal, pulling it forward into a bend — the anorectal angle — which is part of what maintains continence. Squatting straightens that angle considerably; sitting on a standard toilet leaves it partly kinked.
This is the real basis of the footstool advice. Raising the feet brings the position closer to squatting, straightens the angle, and reduces the straining required. It is a genuine mechanical effect, and it helps with constipation and haemorrhoids.
Defecation itself combines relaxation of both sphincters with a Valsalva manoeuvre — hence the rise in blood pressure and the fact that straining can trigger fainting or, rarely, a cardiac event in vulnerable people.
Reading your own stool
Not a delicate topic, and a genuinely informative one.
Normal colour is brown, from stercobilin, a bilirubin breakdown product (Chapter 7.1).
Pale or clay-coloured — bile is not reaching the gut. Obstructive jaundice (Chapter 9.4).
Black and tarry (melaena) — bleeding from the upper gut, digested during transit. This is an emergency. (Iron tablets and bismuth also blacken stool, but not tarry and not with the characteristic smell.)
Fresh red blood — bleeding low down. Usually haemorrhoids or a fissure, and usually benign — but always worth reporting, because colorectal cancer can present the same way and the reassurance is worth having.
Greasy, pale, floating, foul-smelling — fat malabsorption (Chapter 9.3).
Consistency is described using a standard seven-point scale, from hard separate lumps at one end to entirely liquid at the other, with a smooth sausage in the middle as ideal.
Frequency varies enormously between healthy people — anywhere from three times a day to three times a week is normal. What matters is a change from your own pattern, not comparison with anyone else's.
Constipation and diarrhoea
Constipation — hard stool, straining, infrequent, or a sense of incomplete emptying.
Causes: low fibre, low fluid, inactivity, ignoring the urge (which reduces rectal sensitivity over time), pregnancy, hypothyroidism, low potassium or high calcium, and — very commonly — drugs: opioids, iron, calcium channel blockers, antidepressants, and antacids containing aluminium.
Opioid-induced constipation is nearly universal and should be prevented rather than treated, which is why a laxative is prescribed alongside every regular opioid.
Treatment order: fibre and fluid, then bulk-forming laxatives, then osmotic laxatives such as macrogol or lactulose, then stimulants such as senna.
And the fear that laxatives cause dependence is largely unfounded for the modern agents. The concern applied to old-fashioned stimulant abuse; osmotic laxatives can be taken long term safely, and undertreating constipation because of that fear causes real harm.
Diarrhoea — increased frequency or fluid content. Four mechanisms:
Osmotic — unabsorbed solute drawing water in. Lactose intolerance, magnesium-containing laxatives, sorbitol in sugar-free sweets. Stops when you stop eating the substance.
Secretory — the gut actively secretes fluid. Cholera (Chapter 1.4), some toxins, some tumours. Continues even when fasting, which is the distinguishing feature.
Inflammatory — damaged mucosa. Infection, inflammatory bowel disease. Blood and pus present.
Motility — contents moving too fast. Irritable bowel syndrome, hyperthyroidism.
Most acute diarrhoea is infectious and self-limiting, and the treatment is fluid and salt (Chapter 1.4). Antibiotics are rarely needed and often harmful. Antimotility drugs such as loperamide are useful for convenience but should be avoided where there is fever or blood, because slowing the gut retains the pathogen and its toxins.
When to seek help: blood, fever, severe dehydration, symptoms beyond a few days, recent hospital or antibiotic exposure, or recent travel to a high-risk area.
Irritable bowel syndrome
Very common — 10 to 15 percent of people — and often dismissed, which is a mistake.
It is a disorder of gut–brain interaction: altered motility, heightened sensitivity to normal gut sensations, and altered processing of those signals by the brain. There is no structural damage, and that does not make the symptoms less real.
Abdominal pain related to defecation, with a change in stool frequency or form. Bloating is near-universal.
It is a positive diagnosis, not a diagnosis of exclusion, provided the alarm features are absent — blood, weight loss, onset over 50, anaemia, family history of bowel cancer or coeliac disease.
What actually helps, in order of evidence:
The low FODMAP diet — reducing specific fermentable carbohydrates — helps around 50 to 70 percent of people. It is intended as a short elimination phase followed by structured reintroduction, not a permanent restriction, and it needs dietitian support to avoid an unnecessarily narrow long-term diet.
Soluble fibre such as ispaghula helps; insoluble bran often makes it worse, which is the opposite of common advice.
Peppermint oil has reasonable evidence for pain and bloating.
Antispasmodics for pain, loperamide for diarrhoea, laxatives for constipation.
And psychological therapies work genuinely well — cognitive behavioural therapy and gut-directed hypnotherapy have some of the strongest evidence of anything in this list, which reflects the gut–brain mechanism rather than implying the symptoms are imagined.
Low-dose tricyclic antidepressants are used for pain at doses far below antidepressant levels, acting on gut nerve sensitivity.
Inflammatory bowel disease and cancer, briefly
Crohn's disease and ulcerative colitis are covered in Chapter 21.2. The short version: both are autoimmune inflammation of the gut, both are lifelong, and both are now managed well enough that most patients live full lives with modern biologic treatment.
Colorectal cancer is Chapter 19.5, and the encouraging point belongs here: it is one of the most preventable cancers, because it almost always arises from a polyp that takes years to become malignant. Screening — by stool testing or colonoscopy — finds and removes those polyps. Screening programmes reduce colorectal cancer deaths by around 15 to 30 percent, and removing a polyp prevents a cancer that would otherwise have happened.
What the next page fixes
The last section of this Part looks at what the gut's output actually tells a doctor, and pulls together the practical signs from across the Part. Chapter 9.7 covers what your stool, your symptoms and a small number of simple tests reveal about the whole digestive tract — and which findings mean "watch" and which mean "go now".