Depression and the body: pain, fatigue and digestion

“The psychiatrist diagnosed me with depression. But what bothers me most is my back.”

The woman who said this was almost embarrassed. As though it were improper, having been given a psychiatric diagnosis, to talk about her lower back, about her arms aching in the morning, about feeling heavy after every lunch. As though that were a different subject that did not belong in my room.

It does belong. Depression is not a condition that happens in the head and brushes against the body in passing. For a large share of people the physical signs are the most disruptive part, and often the reason they first sat in a waiting room at all – except that they sat in their GP’s waiting room, not a therapist’s.

One boundary is worth clearing up straight away. We are not talking here about physical symptoms that investigations fail to explain; I wrote about those in the piece on what it means when the results come back normal. We are talking about something else: bodily signs that belong to an already established diagnosis of depression. They are not a leftover to be explained elsewhere. They are depression itself, as it shows up in the body.

How common is this really

More common than most people think. A large body of primary care research led by Kurt Kroenke found that depression presents far more often through physical complaints than through a statement about mood. In a well-known World Health Organisation study spanning fifteen cities around the world, the majority of people with depression listed only physical problems at their first visit to a doctor.

This is not evasion, and it is not shame – although both are sometimes in the room. It is simply true that fatigue, pain and poor sleep are more tangible and more urgent than the fact that a person feels empty.

Three routes by which mood is written into the body

When I explain why one condition produces such different signs, I usually draw three routes. None is a complete explanation, but together they cover most of what people describe.

The first is inflammation. In a subset of people with depression, inflammatory markers in the blood are moderately raised – CRP, interleukin 6, TNF-alpha. The experiment in the opposite direction is the interesting one: if healthy volunteers are given a substance that triggers a short-lived inflammatory response, within hours they develop fatigue, slowing, social withdrawal and lowered mood. So inflammation is not only a consequence; it can also cause part of the symptom picture.

The second is the hypothalamic-pituitary-adrenal axis, the system that regulates cortisol. Under chronic stress its daily rhythm flattens: too little rise in the morning, too little settling at night. That accounts for a good deal – from morning stiffness to why someone suddenly wakes up at eleven in the evening.

The third is pain regulation. A pain signal from the body is not a photograph of an injury; the brain amplifies or dampens it as it arrives. That dampening depends largely on the serotonin and noradrenaline pathways running down the spinal cord – the same systems that are altered in depression. Which is why, in depression, the same stimulus genuinely does hurt more.

Pain that is not in your head and is not invented

Of all the physical signs, pain is the one closest to my heart, because it is the one dismissed fastest. People arrive with a headache years old, with lower back pain, with tight shoulders that a massage softens for three days – and somewhere along the way they have been told it is “just nerves”.

Measurement says otherwise. In experiments where pain is induced under controlled conditions, people with depression generally tolerate sustained, dull stimuli less well, even though with brief sharp ones there is sometimes no difference at all. That is not character. That is altered regulation.

The practical consequence matters: pain and mood almost always move together. When one improves the other often does too – though not necessarily at the same time or in the same direction. So with people who have both, I never propose that we “sort out the head first and the body will follow”.

There is a second half to this story, and it is more awkward. Long-standing pain markedly raises the likelihood of depression in its own right – the link is equally strong in both directions. If somebody has got up every morning for three years with pain that has no visible end, that is not the background to their mood, it is their daily life. At that point the question of which came first is usually useless.

Fatigue that sleep does not repair

This is the most common sign and the most misleading. A person sleeps eight hours, sometimes ten, and gets up as though they had worked all night. Then someone asks whether they are sleeping enough – and the conversation heads in the wrong direction.

Depressive fatigue is not about sleep duration. It is a state in which every action costs more than it should. A shower is a project. Replying to a message is a project. Studies measuring effort expenditure in depression show that, given equal options, people more often choose the easier task with the smaller reward – not because they do not care, but because effort in this system genuinely is more expensive.

Alongside it there is almost always sleep of poorer quality, even when there is plenty of it. How that works, and why the body does not cool down at night, I explained in more detail in the piece on insomnia and the nervous system.

Digestion: the other place this shows

The gut is often the first thing to speak up in depression. Reduced or excessive appetite, a feeling of fullness after a few mouthfuls, constipation, bloating, a sensitivity that rises and falls with periods of distress.

There are three explanations and all three are mundane. First, the speed at which food moves through the gut is governed by the autonomic nervous system, which in depression is shifted towards the sympathetic side – slowing digestion and raising the sensitivity of the gut wall. Second, behaviour changes: fewer regular meals, more sugar or alcohol, less movement, less water. Third, a fair number of people with depression also have irritable bowel syndrome; the two conditions occur together considerably more often than chance would predict.

What I think is worth saying: none of this means the gut is “to blame” for depression. Microbiome research is promising and at the same time nowhere near telling anyone what to take. I set out my caution about drawing conclusions from promising findings in the piece on why therapy is harder to research.

When the body slows down or cannot keep still

Less is said about psychomotor changes, which an outside observer often notices before the person does. A slower walk, a quieter and flatter voice, longer pauses before answering, fewer gestures. Or the opposite: restless legs, a fine tremor in the hands, an inability to sit down.

Partners often describe this as “he isn’t the way he used to be”, without being able to say what exactly changed. Naming it clarifies a great deal – not least because slowing is so often mistaken for indifference towards them.

It is also worth knowing that psychomotor slowing is one of the few signs of depression that can be judged fairly reliably from outside, without the person’s own report. That makes it useful with people who say little about their state – older adults, men who learned that this is not discussed, and anyone who struggles to find words for what happens inside. Here the body says what language does not.

Why this is not the same as psychosomatics

The difference is small in words and large in consequences.

With physical symptoms and no findings, the central question is what the symptom means and what sustains the loop between worry, attention and sensation. With the bodily signs of depression something more direct is going on: a diagnosis has been made, and these signs are one of its measures. When the depression recedes, they usually recede with it.

Why does the difference matter? Because it decides where we start. If someone has a diagnosis and their back hurts, it makes no sense to open with the idea that the pain “is telling them something”. It makes sense to treat the depression and track the pain as one of the indicators. The opposite holds when there is no diagnosis and the investigations keep coming back empty. Making that distinction sometimes takes me several sessions, and until it is clear I promise nothing.

What is actually done about it

Nothing exotic, but worth setting out in order.

First: I measure the physical signs. Not loosely, but on a scale of 0 to 10, once a week, alongside mood. After two months it almost always turns out that the two curves move together – and that is more convincing to a person than any explanation of mine.

Second: movement. Not as a moral demand, but as an intervention with a measurable effect on inflammatory markers, sleep and pain. Ten minutes of walking a day that actually happens beats a gym plan that will not.

Third: rhythm. The same waking time, daylight in the morning, regular meals. Dull, which is exactly why it stays undone.

Fourth: a conversation with whoever prescribes. Some antidepressants acting on noradrenaline have a somewhat different profile where pain is also present than those acting mainly on serotonin. That is not my decision and I will not be making it, but it is a question worth asking. I have written about the relationship between medication and therapy in the piece on antidepressants and therapy.

Where I have to be careful

Now the part usually left out of articles about depression.

If you attribute everything physical to depression, you make the same mistake as the person who misses the depression entirely. Fatigue, pain and digestive trouble are also signs of anaemia, thyroid disease, vitamin B12 or D deficiency, diabetes, autoimmune conditions, sleep apnoea and a good deal more. Some of them produce symptoms all but indistinguishable from depression.

So I keep a simple rule: a new physical symptom, or a marked worsening of an old one, goes to a doctor first, not into therapy. I am not the person who will rule out a physical cause. I am not, and I must not be; where the limits of each profession lie is something I set out in the piece on who is allowed to make a diagnosis.

And two more things. The link between inflammation and depression holds for a subgroup, not for everyone – by most estimates somewhere between a quarter and a third. If you have depression without raised inflammatory markers, that does not mean your fatigue is not real; it means this is not the route. And measuring CRP because of depression is not part of routine care today, because no different decision follows from the result.

What to remember

For a large share of people, depression shows up first in the body: as fatigue that rest does not repair, as pain without an injury, and as a gut that rises and falls with mood. These are not side nuisances and they are not imagined. They are part of the same condition, along three reasonably well described routes.

If you have a diagnosis, do not treat the physical signs separately – track them as an indicator of how things are going. If you do not have a diagnosis and something has been dragging you down for months, start with a doctor. Not because the psychological is any less real, but because you need to know what you are dealing with.

And if somebody tells you it is “just nerves”, you can calmly reply that nerves really are in the body – and that this is not the same as “it is nothing”.