Story
Depression & Anxiety · Nutritional Psychiatry
Last updated
In one pass Depression and anxiety are not something you can "just cheer up" out of, and they are not "being dramatic" — they are real changes in the brain and body.
Educational content, not medical advice — consult a clinician.
Story path
Chapter 1
More than feeling sad
Depression and anxiety are not something you can "just cheer up" out of, and they are not "being dramatic" — they are real changes in the brain and body. Like high blood sugar or high blood pressure, they have mechanisms that research is working to explain, and treatments backed by solid evidence.
The current explanation is that several lines act together. Stress that never switches off keeps cortisol (a stress hormone) high, and in animal experiments that makes the branches of nerve cells shrink in the hippocampus (a brain region that handles memory and helps put the brakes on emotion). Inflammatory signals may also reach the brain and divert tryptophan, the raw material for making serotonin. Much of this comes from animal experiments and from associations seen in groups of people; the full picture in humans is still being pieced together.
Because more than one line is involved, a single remedy is often not enough. Nutritional psychiatry (the field that studies how diet relates to mental health) is an add-on, not a substitute: moderate and severe illness needs medication plus psychotherapy, and nothing here replaces seeing a doctor.
Red flags — get help now:
thoughts of suicide, or a planself-harmbeing unable to look after yourselfpsychotic symptoms (hallucinations, delusions)In an emergency: in mainland China, call the national psychological assistance hotline 12356; wherever you are, you can go to your local emergency department.
The current explanation is that several lines act together. Stress that never switches off keeps cortisol (a stress hormone) high, and in animal experiments that makes the branches of nerve cells shrink in the hippocampus (a brain region that handles memory and helps put the brakes on emotion). Inflammatory signals may also reach the brain and divert tryptophan, the raw material for making serotonin. Much of this comes from animal experiments and from associations seen in groups of people; the full picture in humans is still being pieced together.
Because more than one line is involved, a single remedy is often not enough. Nutritional psychiatry (the field that studies how diet relates to mental health) is an add-on, not a substitute: moderate and severe illness needs medication plus psychotherapy, and nothing here replaces seeing a doctor.
Red flags — get help now:
thoughts of suicide, or a planself-harmbeing unable to look after yourselfpsychotic symptoms (hallucinations, delusions)In an emergency: in mainland China, call the national psychological assistance hotline 12356; wherever you are, you can go to your local emergency department.
Numbers · How common, and how many go untreated
It is very common, and very easily treated as a matter of willpower: about 1 in 10 people will go through a serious mood disorder, and in China most of them are never diagnosed or treated. Calling it a character flaw only makes people seek help later and blame themselves more.Major depressive disorder (MDD) and the anxiety disorders (including generalized anxiety disorder, GAD, panic disorder and social anxiety) are the most common psychiatric illnesses of our time. The epidemiology (WHO 2024, and the China Mental Health Survey published by Huang in 2019 in *Lancet Psychiatry*): lifetime prevalence of any depressive disorder in China is about 6.8% (of which MDD is 3.4%), against 5–15% worldwide; any anxiety disorder is about 7.6% in China and 14–20% worldwide; about half of people with MDD or an anxiety disorder have both; and in China more than 80% are undiagnosed and untreated. According to WHO estimates, depression and anxiety rose by another 25–30% worldwide during the pandemic years of 2020–2022.
Clinical · How doctors count, and how you self-score
How is depression counted in the clinic (under the US diagnostic manual, DSM-5)? MDD requires at least 5 symptoms lasting at least 2 weeks, including at least one core symptom — low mood (most of the time) or anhedonia (losing interest in what you used to enjoy). The other symptoms include changes in appetite, changes in sleep, being slowed down or agitated, fatigue, feelings of worthlessness or guilt, trouble concentrating, and thoughts of death or suicide. GAD is excessive anxiety and worry that is hard to control and lasts at least 6 months, plus at least 3 symptoms (restlessness, tiring easily, poor concentration, irritability, muscle tension, insomnia).Self-checks and clinics both commonly use two scales: the PHQ-9 (Patient Health Questionnaire, 9 items, scored 0–27), where 10 or more suggests depression, and the GAD-7 (Generalized Anxiety Disorder scale, 7 items, scored 0–21), where 10 or more suggests anxiety. The Chinese versions of both have been validated, and you can complete a self-rating within 15 minutes. They are screening tools, not a diagnosis.
Chapter 2
How depression develops in the brain
Ask what depression is, and the most popular answer is that serotonin is low. That is not wrong, but at most it covers one stretch of the chain.
The chain researchers have pieced together runs roughly like this. Stress that never switches off makes the adrenal glands pour cortisol into the blood; in animal experiments, long exposure to cortisol makes the branches of nerve cells in the hippocampus (the part of the brain that handles memory and also brakes emotion) shrink, and new cells grow more slowly. Another line is inflammation: one hypothesis holds that once inflammatory signals reach the brain, they both push down the protein that lets neurons grow new branches (BDNF) and divert tryptophan, the raw material for serotonin, down a different metabolic route. This line rests mostly on animal experiments and on associations seen in groups of people.
The chain also explains something odd: antidepressants raise serotonin in the synapse within hours, yet people take weeks to feel better. One leading explanation is that the chemical level changes fast, while regrowing the branches is slow.
That is why treatment often works on several fronts at once. Medication, psychotherapy, exercise, sleep and diet each repair a different stretch; they are not substitutes for one another.
The chain researchers have pieced together runs roughly like this. Stress that never switches off makes the adrenal glands pour cortisol into the blood; in animal experiments, long exposure to cortisol makes the branches of nerve cells in the hippocampus (the part of the brain that handles memory and also brakes emotion) shrink, and new cells grow more slowly. Another line is inflammation: one hypothesis holds that once inflammatory signals reach the brain, they both push down the protein that lets neurons grow new branches (BDNF) and divert tryptophan, the raw material for serotonin, down a different metabolic route. This line rests mostly on animal experiments and on associations seen in groups of people.
The chain also explains something odd: antidepressants raise serotonin in the synapse within hours, yet people take weeks to feel better. One leading explanation is that the chemical level changes fast, while regrowing the branches is slow.
That is why treatment often works on several fronts at once. Medication, psychotherapy, exercise, sleep and diet each repair a different stretch; they are not substitutes for one another.
Mechanism · Models ①② · transmitters and branches
The neuroscience of depression has long since moved beyond the single sentence not enough serotonin. The current mainstream is 4 complementary models; here are the first two.① The monoamine hypothesis (traditional):
Too little serotonin (5-hydroxytryptamine, ), norepinephrine (NE) and dopamine (DA) in the synapse is thought to cause depression.The main action of and is to block these transmitters from being taken back up, so more of them is available in the synapse.The limitation: monoamine levels rise within hours, yet the drugs take 2–4 weeks to work — a sign that simply topping up monoamines is not the whole story.
② The neuroplasticity and BDNF hypothesis:
Brain-derived neurotrophic factor (BDNF) is a protein that helps neurons grow new connections, and it is often found to be low in people with depression, especially in the hippocampus.In animal experiments, chronic stress raises cortisol, fewer new neurons form in the hippocampus, and dendrites (the branches through which neurons receive signals) shrink.One leading explanation is that SSRIs raise BDNF indirectly and promote new neurons, which may explain why the drugs take 2–4 weeks to work; this link comes mainly from animal research.Exercise, learning, sunlight and a nutrient-rich diet are all thought to raise BDNF, with evidence of varying strength.
Mechanism · Model ③ · the line from the gut to the brain
③ The gut-brain axis:Gut microbes are thought to talk to the brain through several routes: the vagus nerve, short-chain fatty acids, endotoxin made by bacteria, and tryptophan metabolism.In observational studies, the gut microbes of people with depression differ from those of healthy people (for example, fewer *Lactobacillus* and *Bifidobacterium*); this is an association and does not show which causes which.Among psychobiotics (probiotics that might affect mood), the most concrete piece of evidence is one strain in one population: *Bifidobacterium longum* NCC3001 lowered depression scores after 6 weeks in 44 adults who had irritable bowel syndrome () together with mild-to-moderate anxiety or depression (Pinto-Sanchez 2017, *Gastroenterology*). That is a population with IBS, not a depression clinic, and the trial did not test *L. helveticus*.Depression also often carries an inflammatory background. Under the inflammation hypothesis, raised inflammatory molecules (, , ) may cross the blood-brain barrier (), set off inflammation in the brain, lower serotonin () production and damage neurons.Dietary interventions are thought to work mainly through this line; that step has not yet been directly confirmed in people.
Mechanism · Model ④ · the stress axis stuck on
④ -axis dysregulation and chronic stress:The hypothalamic-pituitary-adrenal (HPA) axis: under stress, the hypothalamus first releases corticotropin-releasing hormone (CRH), which prompts the pituitary to release adrenocorticotropic hormone (ACTH), which in turn makes the adrenal glands release cortisol.In some people with depression, cortisol stays high for long periods and negative feedback (the brake by which cortisol tells the upstream stations to quiet down) often works poorly; in animal experiments, long-term high cortisol damages the hippocampus.Some people use supplements such as ashwagandha (see Ashwagandha) to try to adjust this axis; its evidence and limits are covered there.
Mechanism · How the four lines twist into one
How the 4 models fit together: some researchers string them into a single chain of hypotheses. Chronic stress first switches on the axis, raising cortisol and inflammation. Inflammation then combines with an unbalanced gut microbiome, letting endotoxin leak into the blood and making the blood-brain barrier more permeable, which sets off inflammation in the brain. That brain inflammation both pushes down BDNF and new neurons and steals the raw material for serotonin (): it switches on an enzyme called indoleamine 2,3-dioxygenase (IDO), which sends tryptophan down the kynurenine pathway instead of into 5-HT. In this hypothesis, several lines push together and the end result is depression. Many links in the chain were measured in animals, and the whole chain has not been fully tested in people.This is also why combined treatment is thought to add up:
repair the monoamine side and indirectly affect BDNF.Exercise is thought to raise BDNF and lower inflammation.Diet is thought to improve the gut microbiome, lower inflammation and supply the raw materials for making neurotransmitters.Psychotherapy works on thinking and behavior.Sleep is thought to affect both BDNF and the HPA axis.
Myth · Will more tryptophan refill serotonin?
The tryptophan-and-serotonin marketing trap:The common line is eat more tryptophan (turkey, milk) and your depression will lift.In reality, tryptophan has to compete with other large neutral amino acids (LNAA) for the same transporter to cross the blood-brain barrier (), so a meal heavy in protein may actually let less tryptophan into the brain and reduce brain production.The old rule that a high-carb meal boosts 5-HT is oversimplified too. supplements (the intermediate step between tryptophan and serotonin) do reach the brain, but they bypass the body's feedback controls, bring cardiovascular and serotonin-syndrome risks, and have weak evidence for depression.The nutritional intervention that trials have actually shown to help is an overall eating pattern (see A trial of eating differently), not a single amino acid.
Chapter 3
A trial of eating differently
Change what you eat for a while, and your mood may really move with it — not a guess, but something a measured, even if it was a small one.
The SMILES trial (Jacka 2017) was the first randomized controlled trial designed to test whether improving diet can treat depression. Of 67 people with moderate to severe depression, half switched, with a dietitian's guidance, to a Mediterranean-style way of eating (whole grains, vegetables, legumes, nuts, fish, olive oil; fewer sweets, refined grains, fried foods and processed meats), while the other half received the same amount of time in social support. After twelve weeks, depression-scale scores had fallen clearly more in the diet group, remission rates were about 32% against 8%, and side effects were almost nil. With only 67 people, and participants who knew which group they were in, it needs to be repeated in larger trials.
Why might changing your food reach the brain? One explanation is that swapping processed foods for whole foods changes the gut microbiome, which may calm inflammatory signaling. That step has not been measured directly in people.
The key word is adjunct: most people in the trial were already taking medication or having psychotherapy. The diet was added on top of that, not used to replace it.
The SMILES trial (Jacka 2017) was the first randomized controlled trial designed to test whether improving diet can treat depression. Of 67 people with moderate to severe depression, half switched, with a dietitian's guidance, to a Mediterranean-style way of eating (whole grains, vegetables, legumes, nuts, fish, olive oil; fewer sweets, refined grains, fried foods and processed meats), while the other half received the same amount of time in social support. After twelve weeks, depression-scale scores had fallen clearly more in the diet group, remission rates were about 32% against 8%, and side effects were almost nil. With only 67 people, and participants who knew which group they were in, it needs to be repeated in larger trials.
Why might changing your food reach the brain? One explanation is that swapping processed foods for whole foods changes the gut microbiome, which may calm inflammatory signaling. That step has not been measured directly in people.
The key word is adjunct: most people in the trial were already taking medication or having psychotherapy. The diet was added on top of that, not used to replace it.
Evidence · How the SMILES trial was designed
**The SMILES trial (Jacka and colleagues, published in 2017 in *BMC Medicine*)** was the first (RCT) in nutritional psychiatry designed to test whether improving diet can treat depression.Design:
N = 67 people with moderate to severe major depression (diagnosed by DSM-IV-TR, with MADRS ≥ 18, and a dietary screen confirming poor diet quality — SMILES never used the PHQ-9). The MADRS is a clinician-rated depression scale on which higher scores mean more severe depression.A modified Mediterranean diet (ModiMedDiet) compared with social support, for 12 weeks.Key point: most participants were already on an or in psychotherapy — this is diet as an add-on, not diet as a replacement.
What ModiMedDiet contained:
Whole grains, vegetables, fruit, legumes, low-fat dairy, nuts, fish or eggs, olive oil, and moderate red meat.Limited: sweets, refined grains, fried foods, processed meat, soft drinks and alcohol.In effect, it is a modified Mediterranean diet that is low in ultra-processed foods ().
Numbers · How much the diet group actually improved
Results:MADRS (Montgomery-Åsberg Depression Rating Scale):Diet group fell by 11 pointsControl group fell by 4 pointsA 7-point difference, which the researchers considered clinically meaningfulRemission rate (MADRS < 10):Diet group 32%Control group 8%Number needed to treat, = 4 (for about every 4 people treated, 1 more reaches remission). This figure comes from a single small trial and cannot be set directly against numbers from large drug .Anxiety scores also improved.Side effects: almost none.
Evidence · Did anyone replicate it
Replication studies:HELFIMED 2019 (Parletta; 152 recruited, 95 completing at 3 months): a Mediterranean diet plus fish oil compared with social groups — depression scores fell further (p = 0.03), and the difference held at 6 months. ⚠️ The fish oil is part of the intervention, so it is not a diet-only replication.AMMEND 2022 (Bayes, 72 completers): Australian men aged 18–25, 12 weeks of a Mediterranean diet compared with a befriending control, with a 14.4-point difference between groups on the Beck Depression Inventory (BDI-II). ⚠️ It is an open-label (both participants and researchers knew the groups), single-site , not a .
What can be said so far:
Three randomized trials (SMILES, HELFIMED, AMMEND) all found greater improvement in the diet group among people who already had depression, pointing the same way; but all are small and participants knew their group, so they are not yet conclusive.Diet cannot replace medication or psychotherapy, but when added on top of existing treatment, the trials saw extra improvement.For prevention (in healthy people): an umbrella review by Lane, published in 2024 in the *BMJ*, pooled observational studies and found that people who ate more ultra-processed food had a higher risk of depression — an association, which does not show that the food caused it.
lane-2024-bmj-upf-meta
Evidence · Fish oil, vitamin D and folate
Individual nutrients (single-nutrient evidence):① Omega-3 (mainly ):
The higher the EPA dose, the larger the effect, and the benefit is clearer in people already taking an antidepressant (Mocking 2016 : 13 , 1,233 people, overall standardized mean difference, SMD, 0.398, p = 0.006). ⚠️ The paper tested the ratio of EPA to as a moderating factor, and it was not significant — so the product rule that EPA must make up more than 60% does not come from this paper.On its own the effect is small; added to an it is more noticeable.
② Vitamin D:
In Anglin's 2013 meta-analysis, people with low blood levels of vitamin D had depression more often (an observed association).But randomized trials of vitamin D supplements for depression disagree — the link may be association rather than cause, or supplements may help only people who are deficient.
③ Folate and vitamin B12:
People low in folate or B12 (especially older adults, vegans, or people with gene variants) have depression more often (an association).A trial by Papakostas, published in 2012 in the *American Journal of Psychiatry*, added L- (the US prescription product Deplin) to an SSRI and saw some extra improvement; it needs to be repeated in more trials.
Evidence · Magnesium and zinc
④ Magnesium:An unblinded randomized crossover trial by Tarleton in 2017, in adults with mild to moderate depression, saw depression and anxiety scores fall after magnesium supplementation; it needs to be repeated.The mechanism may involve NMDA receptors (glutamate receptors that excite nerve cells), (the main calming neurotransmitter) and the stress axis, none of which has been confirmed.
⑤ Zinc:
Low zinc is associated with depression (a 2018 by Wang); whether zinc supplements improve depression is less clear, and the evidence is limited.
Safety · The red line when taken with a prescription
Warnings:Taking , or St John's wort together with an can cause serotonin syndrome (too much serotonin in the body, which can be dangerous); avoid the combination.L-tryptophan: its entry into the brain is limited by competition for transport; amounts within an ordinary diet are fine, and the evidence for high-dose supplements is weak.Before combining any nutritional intervention with a prescription drug, talk it over with your psychiatrist first; do not add things on your own.
Chapter 4
Therapy and medication both work
Depression and anxiety can be treated, and by more than one route. Psychotherapy and medication are both first-line options. Which one to start with is not about which is more advanced; it depends on how severe your symptoms are and what you can get access to.
Psychotherapy works at the level of thoughts and behavior. The strongest evidence is for cognitive behavioral therapy (), often the first choice for mild to moderate illness, with long-term results as good as medication; mindfulness-based cognitive therapy (MBCT) is used mainly to prevent relapse.
Medication changes the chemical environment in the synapse. The most commonly prescribed class is the selective serotonin reuptake inhibitors (). After serotonin is released into the gap between nerve cells, it would normally be taken back up by the cell that released it; these drugs block that reuptake channel so serotonin stays around a little longer. One leading explanation is that real improvement comes from the slow rebuilding of nerve connections over the following weeks, which is why you feel nothing on the day you take it — and why it is so often mistaken for not working.
Psychotherapy works at the level of thoughts and behavior. The strongest evidence is for cognitive behavioral therapy (), often the first choice for mild to moderate illness, with long-term results as good as medication; mindfulness-based cognitive therapy (MBCT) is used mainly to prevent relapse.
Medication changes the chemical environment in the synapse. The most commonly prescribed class is the selective serotonin reuptake inhibitors (). After serotonin is released into the gap between nerve cells, it would normally be taken back up by the cell that released it; these drugs block that reuptake channel so serotonin stays around a little longer. One leading explanation is that real improvement comes from the slow rebuilding of nerve connections over the following weeks, which is why you feel nothing on the day you take it — and why it is so often mistaken for not working.
Clinical · The psychotherapy options
First-line: psychotherapy (often the first choice for mild to moderate illness):Cognitive behavioral therapy (): the evidence comes from a large number of randomized trials and is of high certainty; usually 8–20 sessions, with long-term results as good as medication.Interpersonal therapy (IPT): suited to people whose problems center on relationships.Mindfulness-based cognitive therapy (MBCT): its evidence for preventing relapse comes from several randomized trials.Mindfulness and acceptance and commitment therapy (ACT): supported by randomized trials for anxiety, with moderate-to-high certainty.Digital CBT (iCBT): CBT delivered on online platforms; not a full substitute for a real therapist, but clearly better than no treatment.
Clinical · The drug options, including newer ones
First-line: medication:(fluoxetine, paroxetine, sertraline, citalopram, escitalopram): take 2–4 weeks to work. Cipriani's 2018 network compared the commonly used antidepressants and found every one more effective than placebo for the acute treatment of major depression in adults. (venlafaxine, duloxetine): block the reuptake of both serotonin and norepinephrine (NE).Mirtazapine: often used for people with poor appetite and marked insomnia, including older adults.Bupropion: less effect on sexual function, and also used to help people stop smoking.Tricyclic antidepressants (TCAs): older drugs that work but have more side effects, and are now rarely first-line.Monoamine oxidase inhibitors (): rarely used now.
Newer drugs (2020s):
Esketamine (Spravato) nasal spray: for treatment-resistant major depression, with a fast onset (hours to days); approved by the US FDA in 2019.Brexanolone and zuranolone: for postpartum depression, acting on -A receptors.Psychedelic research (psilocybin, MDMA): trials are ongoing, some results are positive, and regulation varies by country — an important new direction, but far from widespread clinical use.
Clinical · SSRI myths, non-drug levers, when to get help
Common misconceptions about :"SSRIs change your personality and are addictive": not accurate — they are not addictive drugs, but stopping has to be done by tapering slowly (otherwise discontinuation symptoms such as weight changes, dizziness or "brain zaps" can occur)."SSRIs cause sexual side effects": this is real, affecting 30–50% of some patients; alternative drugs exist (bupropion, mirtazapine)."SSRIs are slow, so they don't work": the standard window to watch is 2–4 weeks, and a full assessment should come at 6–8 weeks.
Exercise: the antidepressant evidence comes from several randomized trials and :
A common recommendation is 150 minutes a week of moderate aerobic exercise.Cooney's 2013 Cochrane meta-analysis: exercise against control gave a standardized mean difference (SMD, an effect size that puts different scales on one ruler; a negative value means depression scores fell) of −0.62, a moderate effect. But when only the six most rigorous trials were kept, it dropped to −0.18 and was no longer significant — a caveat the Cochrane authors wrote themselves. In direct comparisons with medication there was no significant difference.Heissel's 2023 meta-analysis in *BJSM* (41 , 2264 people) found a larger effect (SMD −0.95), and −0.67 in the subset of trials at low risk of bias.Possible mechanisms include BDNF, endorphins, a sense of self-efficacy, sleep and social contact.The three elements are intensity, frequency and persistence; a 30-minute walk is easier to keep up than an occasional high-intensity session.
Light therapy: a first-line treatment for seasonal affective disorder (SAD, depression that recurs in winter) — 30 minutes in front of a 10,000 lux light box in the morning. For non-seasonal depression it can be used as an add-on; some randomized trials support it, with moderate certainty.
Sleep: depression and insomnia make each other worse, and research supports the link in both directions (see Insomnia; the effects of shift work are covered in Shift Work). Cognitive behavioral therapy for insomnia () does not conflict with SSRIs, and the two can be used together.
Social support and relationships: isolation is thought to be one of the important risk factors for depression that can be changed. What matters is not simply seeing friends more, but meaningful connection with other people.
When to see a professional:
PHQ-9 ≥ 10 or GAD-7 ≥ 10: see a psychiatrist or a counselor.Symptoms lasting ≥ 2 weeks that affect work and daily life: the same.Thoughts of suicide → seek medical help immediatelyIf adjusting things on your own has not helped for a long time: do not blame yourself; go straight to professional help.
Key reminder: depression and anxiety are not a lack of willpower or being dramatic; they are illnesses with a neurobiological basis. Comfort such as "just think positive" or "what is there to worry about" misses the point entirely and can deepen guilt. Stigma is thought to be one of the main reasons so few people in China seek care.
Chapter 5
Self-check and when to get help
Not sure whether this applies to you? Measure it first. The PHQ-9 and the GAD-7 are two public questionnaires you can take online, with a score in a few minutes. They are not a diagnosis; they answer one question only: is this something to adjust on your own, or something to get help with?
Your score decides which path you take next:
0–4: none or minimal — keep up what you are doing5–9: mild — start with lifestyle changes plus counseling10–14: moderate — strongly advised to see a professional15+: severe — seek care now
The higher the score, the less you should carry it alone.
Suicide risk: in mainland China, call the national psychological assistance hotline 12356 right away (one national number, routed to your local line); Beijing Psychological Crisis Research and Intervention Center: 010-82951332; Shanghai mental-health hotline: 021-12320-5. Wherever you are, you can go to your local emergency department at any time. ⚠️ The national standard requires 12356 to answer at least 18 hours a day, not 24. If you cannot get through late at night, that does not mean no one will help you — in mainland China, call 120 directly, or go to the nearest hospital emergency department. Emergency departments are open 24 hours.
Your score decides which path you take next:
0–4: none or minimal — keep up what you are doing5–9: mild — start with lifestyle changes plus counseling10–14: moderate — strongly advised to see a professional15+: severe — seek care now
The higher the score, the less you should carry it alone.
Suicide risk: in mainland China, call the national psychological assistance hotline 12356 right away (one national number, routed to your local line); Beijing Psychological Crisis Research and Intervention Center: 010-82951332; Shanghai mental-health hotline: 021-12320-5. Wherever you are, you can go to your local emergency department at any time. ⚠️ The national standard requires 12356 to answer at least 18 hours a day, not 24. If you cannot get through late at night, that does not mean no one will help you — in mainland China, call 120 directly, or go to the nearest hospital emergency department. Emergency departments are open 24 hours.
In practice · What to do at each score band
I might have depression or anxiety: self-check plus actionStep 1 · Self-check (5 minutes):
Take the two questionnaires online (in China, they are available on public health-information platforms and in some apps).Score bands: 0–4 none or minimal, 5–9 mild, 10–14 moderate, 15 or more severe.
Step 2 · Follow the path for your severity:
Mild (PHQ-9 < 10, little effect on daily life):
The 8 lifestyle levers (see Step 3).Digital (in China, platforms such as Simple Psychology, KnowYourself or HaoXinQing).Re-take the PHQ-9 once a month.If there is no improvement, step up.
Moderate (PHQ-9 10–14):
Professional counseling or therapy (CBT preferred).Medication can be considered (discuss with a doctor; it is not mandatory).Lifestyle changes alongside.Re-assess every 2–4 weeks.
Severe (PHQ-9 ≥ 15):
See a psychiatrist or a psychosomatic-medicine department soon.Medication (an or ) combined with psychotherapy is usual.Suicide risk is assessed (for example with the Columbia Suicide Severity Rating Scale).Some people need a brief hospital stay.
In practice · Steps 3–4: lifestyle and nutrition
Step 3 · The 8 lifestyle levers (in order of payoff for effort):1. Exercise: 150 minutes a week of moderate aerobic activity, with depression scores falling clearly; the evidence comes from several randomized trials, and in Cooney's 2013 Cochrane there was no significant difference in direct comparisons with medication.
2. Sleep: 7–9 hours on a regular schedule, with insomnia treated by .
3. Diet: a Mediterranean, DASH or low-ultra-processed-food () pattern (see SMILES and the other two small trials).
4. Sunlight and the outdoors: morning daylight, natural surroundings, and vitamin D.
5. Social contact: meaningful connections with other people (isolation is an important risk factor).
6. Stop or cut down alcohol: it lifts mood briefly but worsens depression in the long run.
7. Less screen time and social media: heavy long-term social-media use is linked with signs of anxiety and depression.
8. Mindfulness and meditation: apps (Headspace, Calm, Yinian) plus in-person classes.
Step 4 · Nutritional support (an add-on, not a replacement):
Omega-3 (mainly ): 1–2 g a day. What Mocking 2016 supports is a higher EPA dose giving a larger effect, not the shelf rule that EPA must make up 60% (the ratio was not significant as a moderating factor).Vitamin D: ≥ 800–2000 a day for people who are deficient.B12 and folate: monitor in long-term vegetarians, older adults and people with gene variants.Magnesium: 300–400 mg a day (glycinate or citrate); the top of that range is above the tolerable upper intake level () for supplemental magnesium, so take it under a doctor's guidance.Zinc: 8–15 mg a day for people who are deficient (vegetarians, people who eat little red meat).Avoid: combining , St John's wort or with an (serotonin syndrome).
In practice · Step 5: long-term care and cautions
Step 5 · Long-term maintenance:Keep using the skills you learned in after your symptoms ease.To prevent relapse: MBCT, regular exercise and a steady daily rhythm.Taper medication slowly, together with your doctor; after remission it is usually continued for a while (a common rule of thumb is at least 8–12 months) before tapering.Learn your early relapse signals — changes in sleep, changes in appetite, fading interest — and act early when they appear.
A few cautions:
Influencer psychology advice mostly comes from people without professional credentials; treat it with care.Some emotion-management courses are commercial products that overpromise and cannot replace real treatment.Antidepressant supplements mostly have weak evidence and come with a commercial markup.Traditional Chinese medicine for depression: individual formulas (such as Xiaoyao San) show some signals, but the evidence is not strong enough for first-line use.
Worth remembering:
Depression and anxiety are illnesses, not weak character, weak will or melodrama.Stigma is thought to be one of the main reasons so few people in China seek care; you are not facing this alone.Lifestyle and nutrition are add-ons, not replacements for medication or psychotherapy.With early intervention, complete treatment and long-term maintenance, most people improve clearly.Finding the right doctor or therapist may take 2–3 tries; do not give up because the first one was not a good fit.Recovery or remission does not mean perfection — it means getting back to a state where you can live the life you want.
In practice · Finding therapy in China
"I have depression, but I'm afraid to see a doctor" — surveys show that only 9.5% of people with depression in China get care, against 40–50% in Western countries. Stigma, not knowing where to go, and worry about a record are the three main barriers.Where the stigma comes from, point by point:
"Seeing a psychologist means I'm crazy": not true. Depression is an illness with a biological basis that, like diabetes, needs treatment."My employer will find out": in China, records at public hospitals are in principle not passed on to employers."It will hurt my chances of marriage or promotion": some careers (civil service, pilots) have restrictions on a psychiatric history, but most ordinary jobs have no explicit restrictions."Others tough it out, so I can too": do not let that comparison carry you along. What you cannot see is that others may also be quietly getting treatment.
Practical routes to counseling and therapy in China:
A. Public hospitals (insurance, prescriptions, suitable for severe cases):
Psychiatry, psychology or psychosomatic-medicine departments in general hospitals (most top-tier hospitals have them).Specialist hospitals: Beijing Anding Hospital, Shanghai Mental Health Center, Nanjing Brain Hospital and others.Pros: insurance coverage and prescriptions; cons: short appointments (10–15 minutes), few psychotherapy resources, and waiting lists.
B. Private counseling (, talk therapy):
Online platforms such as Simple Psychology, Yi Xinli and KnowYourself.Look for credentials such as national Level-2 or Level-3 counselor.Fees: ¥300–1500 per 50 minutes.Frequency: once a week for 12–20 weeks.Pros: enough time, genuine psychotherapy, good privacy; cons: out of pocket, uneven quality, no prescriptions.
C. Online video counseling and digital CBT (apps; fine as a start):
The same platforms as above, by video and text.Apps: HaoXinQing, XinQing, Woebot, Headspace, Calm.Advantages: cheap, available any time, anonymous; limits: moderate or more severe illness needs a real therapist.
How to choose a counselor or doctor:
1. Credentials: national Level-2 or Level-3 counselor, or a licensed psychiatrist.
2. Approach: CBT (the most evidence), psychodynamic therapy, EMDR, mentalization and others.
3. How the first session feels: can you relax enough to talk within 10 minutes? If not, switch.
4. No hard sell of intensive packages, no selling courses, no insisting on private WeChat contact.
5. If you still feel no improvement after 2–3 sessions, switch: it is not your fault; it is a question of fit.
When to move up to psychiatry and medication:
PHQ-9 ≥ 15 (severe).Thoughts of suicide or self-harm.Serious impact on work, study or daily life.No clear improvement after 3 months of counseling.Bipolar disorder (a history of mania or hypomania) should be assessed by a psychiatrist and usually needs a mood stabilizer.
What family and friends can do:
Listening is not the same as solving; do not rush to give advice.Phrases like "you need to pull yourself together" or "stop overthinking" deepen stigma; try to avoid them.Encourage them to seek care and go along to appointments; question less.Learn the basics about depression and anxiety.Look after yourself too; caregiver burnout is real.
Related topics: insomnia is often an early warning sign of depression and often comes with it (see Insomnia); the fall in estrogen () around perimenopause and depression risk; premenstrual dysphoric disorder (PMDD, covered in Menstrual Cycle); sleep apnea (Obstructive Sleep Apnea); and adaptogen supplements such as rhodiola (Rhodiola).
References · 12
- World Health Organization. (2024). Mental health: strengthening our response. WHO Fact sheet. www.who.int/news-room/fact-sheets/detail/mental-health-strengthening-our-response
- Huang, Y., Wang, Y., Wang, H., Liu, Z., Yu, X., Yan, J., et al. (2019). Prevalence of mental disorders in China: a cross-sectional epidemiological study. The Lancet Psychiatry, 6(3), 211-224. 10.1016/S2215-0366(18)30511-X
- Malhi, G. S., & Mann, J. J. (2018). Depression. The Lancet, 392(10161), 2299-2312. 10.1016/S0140-6736(18)31948-2
- Cryan, J. F., O'Riordan, K. J., Cowan, C. S. M., Sandhu, K. V., Bastiaanssen, T. F. S., Boehme, M., et al. (2019). The microbiota-gut-brain axis. Physiological Reviews, 99(4), 1877-2013. 10.1152/physrev.00018.2018
- Pinto-Sanchez, M. I., Hall, G. B., Ghajar, K., Nardelli, A., Bolino, C., Lau, J. T., et al. (2017). Probiotic Bifidobacterium longum NCC3001 reduces depression scores and alters brain activity: a pilot study in patients with irritable bowel syndrome. Gastroenterology, 153(2), 448-459.e8. ⚠️ SCOPE: one strain, one population — 44 adults with IBS (diarrhoea or mixed) AND mild-to-moderate anxiety and/or depression, 6 weeks, double-blind. It is not evidence in a depression clinic population, and it did not test L. helveticus. 10.1053/j.gastro.2017.05.003
- Jacka, F. N., O'Neil, A., Opie, R., Itsiopoulos, C., Cotton, S., Mohebbi, M., et al. (2017). A randomised controlled trial of dietary improvement for adults with major depression (the SMILES trial). BMC Medicine, 15, 23. 67 adults with major depression (33 diet support, 34 social-support control), 12 weeks, as an adjunct to existing treatment (55 were on psychotherapy and/or drugs). MADRS improved more with diet support (Cohen's d -1.16); remission (MADRS < 10) 32.3% (10 of 31) vs 8.0% (2 of 25), NNT 4.1 (2.3-27.8) (abstract, PMID 28137247). 10.1186/s12916-017-0791-y
- Mocking, R. J. T., Harmsen, I., Assies, J., Koeter, M. W. J., Ruhé, H. G., & Schene, A. H. (2016). Meta-analysis and meta-regression of omega-3 PUFA supplementation for major depressive disorder. Translational Psychiatry, 6(3), e756. 10.1038/tp.2016.29
- Bayes, J., Schloss, J., Sibbritt, D. (2022). The effect of a Mediterranean diet on the symptoms of depression in young males (the “AMMEND: A Mediterranean Diet in MEN with Depression” study): a randomized controlled trial. The American Journal of Clinical Nutrition, 116(2), 572-580. AMMEND: a 12-week open-label single-site RCT in 72 Australian men aged 18-25 with moderate-severe depression, befriending control. It is a single trial, not a pooled review of other trials; its year is 2022 and its first author is Bayes. The story used to list it as a 2024 review by a different author. 10.1093/ajcn/nqac106
- Parletta, N., Zarnowiecki, D., Cho, J., Wilson, A., Bogomolova, S., Villani, A., et al. (2019). A Mediterranean-style dietary intervention supplemented with fish oil improves diet quality and mental health in people with depression: A randomized controlled trial (HELFIMED). Nutritional Neuroscience, 22(7), 474-487. HELFIMED: Mediterranean diet PLUS fish oil versus social groups — the fish oil is part of the intervention, so it is not a clean replication of a diet-only trial. 152 recruited, 95 completed at 3 months; depression fell more in the diet arm (p = 0.03) and held at 6 months. 10.1080/1028415X.2017.1411320
- Cooney, G. M., Dwan, K., Greig, C. A., Lawlor, D. A., Rimer, J., Waugh, F. R., et al. (2013). Exercise for depression. Cochrane Database of Systematic Reviews, (9), CD004366. 10.1002/14651858.CD004366.pub6
- Heissel, A., Heinen, D., Brokmeier, L. L., Skarabis, N., Kangas, M., Vancampfort, D., et al. (2023). Exercise as medicine for depressive symptoms? A systematic review and meta-analysis. British Journal of Sports Medicine, 57(16), 1049-1057. 10.1136/bjsports-2022-106282
- Cipriani, A., Furukawa, T. A., Salanti, G., Chaimani, A., Atkinson, L. Z., Ogawa, Y., et al. (2018). Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis. The Lancet, 391(10128), 1357-1366. ⚠️ ITS EFFECT METRIC IS THE ODDS RATIO FOR RESPONSE — it reports neither Cohen's d nor an NNT. The site used to compare a single trial's d, and a single trial's NNT, against numbers attributed to this paper that are not in it. Do not put it on the same ruler as a small single-site trial. 10.1016/S0140-6736(17)32802-7