Blood Tests for Mental Health
Before assuming it's “all in your head,” check what's in your blood. Dozens of physical conditions produce symptoms indistinguishable from anxiety, depression, and other mental health disorders.
Why Your Psychiatrist Might Order Blood Tests
Depression, anxiety, brain fog, and mood swings are real and debilitating — regardless of their cause. But an increasing body of evidence shows that physical conditions are responsible for a significant proportion of psychiatric presentations. A landmark study in the Archives of Internal Medicine found that up to 46% of patients presenting with psychiatric symptoms had an underlying medical condition contributing to or causing their symptoms.
This does not mean mental illness is not real, or that finding a physical cause invalidates the suffering. It means that a comprehensive evaluation should include blood tests to rule out treatable physical contributors before — or alongside — psychiatric treatment. Many of these conditions are common, easily tested, and highly treatable once identified.
The Royal Australian and New Zealand College of Psychiatrists (RANZCP) guidelines recommend baseline blood tests including thyroid function, full blood count, iron studies, B12, folate, and fasting glucose as part of the initial assessment of depression and anxiety. Yet many patients receive a prescription without ever having these tests done.
Physical Conditions That Mimic Mental Illness
The following conditions produce symptoms that are clinically indistinguishable from psychiatric disorders. All are detectable through blood tests. Some are remarkably common — iron deficiency alone affects 30% of menstruating women.
| Condition | What It Mimics | Key Blood Test | Prevalence |
|---|---|---|---|
| Hypothyroidism | Depression, fatigue, brain fog, weight gain | TSH, Free T4 | 1 in 20 adults |
| Hyperthyroidism | Anxiety, panic attacks, insomnia, tremor | TSH, Free T4, Free T3 | 1 in 50 adults |
| Iron deficiency | Anxiety, ADHD, panic, restless legs | Ferritin, Iron Studies | 30% of menstruating women |
| B12 deficiency | Depression, psychosis, dementia | B12, Active B12 | 10-15% of over 60s |
| Vitamin D deficiency | Depression, seasonal mood changes | 25-OH Vitamin D | 25% of adults |
| Coeliac disease | Depression, anxiety, brain fog | tTG-IgA + Total IgA | 1 in 70 (80% undiagnosed) |
| Pre-diabetes | Anxiety, mood swings, panic | HbA1c, Fasting Glucose | 2 million Australians |
| Cushing's syndrome | Depression, anxiety, psychosis | Morning Cortisol | Rare (2-3 per million) |
| Hyperparathyroidism | Depression, anxiety, confusion | Calcium, PTH | 1 in 500 women over 50 |
| Chronic inflammation | Treatment-resistant depression, fatigue | CRP / hs-CRP | 25-35% of depressed patients |
10 Blood Tests That Can Affect Your Mental Health
Thyroid Function (TSH, Free T4, Free T3)
What it mimics: Hypothyroidism mimics depression: fatigue, weight gain, low mood, poor concentration, and loss of interest. Hyperthyroidism mimics anxiety disorders and panic attacks: racing heart, tremor, restlessness, insomnia, irritability, and a constant sense of dread.
The mechanism: Thyroid hormones regulate the metabolic rate of every cell in your body, including neurons. T3 directly influences serotonin, norepinephrine, and GABA production in the brain. When thyroid function drops, neurotransmitter synthesis slows — producing symptoms clinically indistinguishable from major depressive disorder. When thyroid function is excessive, the nervous system becomes hyperexcitable, producing symptoms identical to generalised anxiety disorder.
How common: Thyroid disorders affect approximately 1 in 20 Australians. Subclinical hypothyroidism (mildly elevated TSH with normal T4) affects up to 10% of women over 50 and is frequently missed because symptoms are attributed to ageing, menopause, or depression. Studies show that 10-15% of patients diagnosed with treatment-resistant depression actually have undiagnosed hypothyroidism.
Clinical note: TSH alone is not always sufficient. A normal TSH with low Free T3 (the biologically active form) can still cause depressive symptoms — this is sometimes called "low T3 syndrome" and is common in chronic illness, calorie restriction, and high-stress states. If your TSH is normal but you have classic thyroid symptoms, ask your GP about Free T3 and thyroid antibodies. Hashimoto's thyroiditis (autoimmune) can cause fluctuating thyroid levels that produce alternating anxiety and depression.
Iron Studies (Ferritin, Serum Iron, TIBC, Transferrin Saturation)
What it mimics: Iron deficiency mimics anxiety (restlessness, palpitations, irritability, poor sleep), panic disorder (breathlessness, heart racing, dizziness), ADHD (poor concentration, restless legs, inability to sit still), and depression (fatigue, apathy, brain fog). In children and adolescents, iron deficiency is associated with behavioural problems frequently misdiagnosed as ADHD.
The mechanism: Iron is essential for dopamine synthesis — it is a cofactor for tyrosine hydroxylase, the rate-limiting enzyme in dopamine production. Low iron means low dopamine, which directly impairs motivation, reward processing, concentration, and impulse control. Iron is also required for myelin production (the insulation around nerve fibres), oxygen transport to the brain, and the electron transport chain that produces cellular energy. A brain running on low iron is literally under-powered.
How common: Iron deficiency is the most common nutritional deficiency worldwide, affecting up to 30% of menstruating women in Australia. Ferritin below 30 ug/L is associated with fatigue, cognitive impairment, and mood disturbance — even though many labs list the "normal" range starting at 15-20 ug/L. Some psychiatrists now consider optimal ferritin for mental health to be above 50 ug/L.
Clinical note: Ferritin is an acute-phase reactant — it rises during inflammation, infection, and liver disease, which can mask true iron deficiency. If you have elevated CRP alongside a "normal" ferritin of 30-50 ug/L, your actual iron stores may be lower than the number suggests. Request iron studies (full panel: ferritin, serum iron, TIBC, transferrin saturation) rather than ferritin alone. A transferrin saturation below 20% with symptoms strongly suggests functional iron deficiency regardless of ferritin level.
Vitamin B12 and Active B12
What it mimics: B12 deficiency mimics depression (fatigue, apathy, emotional flatness, poor memory), psychosis (paranoia, hallucinations, delusions in severe cases — historically called "megaloblastic madness"), dementia (cognitive decline, confusion, personality change), and peripheral neuropathy (numbness, tingling, balance problems). Severe B12 deficiency can cause irreversible neurological damage if untreated.
The mechanism: B12 is essential for methylation — the biochemical process that produces serotonin, dopamine, norepinephrine, and melatonin from their amino acid precursors. Without adequate B12, you cannot efficiently produce the neurotransmitters that regulate mood, sleep, motivation, and cognition. B12 also maintains the myelin sheath protecting nerve fibres; deficiency causes demyelination, producing neuropsychiatric symptoms that can precede anaemia by years. The methylation pathway also regulates homocysteine — elevated homocysteine is independently associated with depression and cognitive decline.
How common: B12 deficiency affects 10-15% of adults over 60 (due to declining stomach acid production needed for absorption), but is increasingly recognised in younger adults, particularly those taking metformin, proton pump inhibitors (PPIs), or following vegan/vegetarian diets. Standard serum B12 levels can be normal while tissue-level deficiency exists — Active B12 (holotranscobalamin) and methylmalonic acid are more sensitive markers.
Clinical note: The "normal" range for serum B12 (typically 150-600 pmol/L) is controversial. Neuropsychiatric symptoms can occur at levels in the low-normal range (150-300 pmol/L). If your B12 is below 300 pmol/L and you have mood or cognitive symptoms, a trial of B12 supplementation is reasonable regardless of what the lab labels as "normal." Active B12 (holotranscobalamin) is a more accurate test if available. Nitrous oxide (laughing gas) inactivates B12 — recreational use can precipitate acute B12 deficiency psychosis.
Vitamin D (25-Hydroxyvitamin D)
What it mimics: Vitamin D deficiency is associated with depression (particularly seasonal affective disorder), anxiety, impaired cognition, and fatigue. Meta-analyses show that vitamin D supplementation has a modest but statistically significant antidepressant effect in people who are deficient. The seasonal pattern of vitamin D synthesis closely mirrors the seasonal pattern of depression in temperate climates.
The mechanism: Vitamin D receptors are found throughout the brain, concentrated in areas critical for mood regulation: the hippocampus, prefrontal cortex, cingulate gyrus, and hypothalamus. Vitamin D modulates the expression of genes involved in serotonin synthesis (tryptophan hydroxylase 2) and influences the production of brain-derived neurotrophic factor (BDNF), which supports neuronal survival and plasticity. Vitamin D also has powerful anti-inflammatory effects in the brain — neuroinflammation is increasingly recognised as a driver of depression.
How common: An estimated 1 in 4 Australian adults are vitamin D deficient (below 50 nmol/L), rising to 1 in 3 during winter in southern states. Risk factors include dark skin, sun avoidance, office work, obesity (vitamin D is sequestered in fat tissue), malabsorption conditions, and age over 70. People with depression are more likely to be vitamin D deficient, though causality remains debated — the relationship is likely bidirectional (depression causes indoor behaviour which worsens deficiency).
Clinical note: The optimal level for mental health is debated. Most guidelines recommend above 50 nmol/L, but some psychiatric researchers suggest above 75 nmol/L for optimal brain function. In Australia, vitamin D testing is bulk billed only for high-risk groups (osteoporosis, malabsorption, dark skin, veiled dress, limited sun exposure). Your GP can request it if there is a clinical indication. Note: Australian units are nmol/L — most US-based online resources use ng/mL. To convert, divide nmol/L by 2.5 (e.g., 75 nmol/L = 30 ng/mL).
Folate (Vitamin B9)
What it mimics: Folate deficiency mimics depression, cognitive impairment, irritability, and insomnia. Low folate is consistently found in depressed patients — studies show that people with low folate are up to 3 times more likely to be diagnosed with depression. Folate deficiency also reduces the effectiveness of antidepressant medications, particularly SSRIs.
The mechanism: Folate is essential for the methylation cycle alongside B12. It provides the methyl groups needed to convert homocysteine to methionine, which is then converted to S-adenosylmethionine (SAMe) — the universal methyl donor your brain uses to synthesise serotonin, dopamine, norepinephrine, and melatonin. The active form of folate (L-methylfolate, or 5-MTHF) crosses the blood-brain barrier and directly participates in neurotransmitter production. Approximately 10-15% of the population carry an MTHFR gene variant that impairs folate metabolism, potentially increasing susceptibility to folate-responsive depression.
How common: Folate deficiency is less common than B12 deficiency in Australia due to mandatory folic acid fortification of bread flour since 2009. However, inadequate intake still occurs in people who avoid grain products, those with malabsorption conditions (coeliac disease, Crohn's), heavy alcohol consumers, and those taking medications that interfere with folate metabolism (methotrexate, some anticonvulsants, trimethoprim).
Clinical note: L-methylfolate (the active form) is used adjunctively with antidepressants, particularly in patients who have not responded to SSRIs alone. This is an evidence-based approach, not a fringe treatment — it is included in some treatment-resistant depression algorithms. Red cell folate is a better measure of long-term folate status than serum folate (which fluctuates with recent intake). If your serum folate is in the low-normal range (7-12 nmol/L) and you have depression, red cell folate provides a more complete picture.
Blood Glucose and HbA1c
What it mimics: Reactive hypoglycaemia (blood sugar crashes 2-4 hours after eating) mimics panic attacks: sudden onset of racing heart, sweating, trembling, dizziness, confusion, and intense fear. Chronic blood sugar dysregulation is associated with anxiety, irritability, mood swings, and depression. Diabetes doubles the risk of depression, and depression doubles the risk of diabetes — a bidirectional relationship.
The mechanism: The brain consumes approximately 20% of the body's glucose despite being only 2% of body weight. When blood sugar drops rapidly (reactive hypoglycaemia), the brain triggers a counter-regulatory stress response — adrenaline and cortisol surge, producing symptoms identical to a panic attack. Chronically elevated blood sugar (pre-diabetes and diabetes) damages small blood vessels in the brain, promotes neuroinflammation, and impairs neuroplasticity. Insulin resistance in the brain reduces serotonin availability and is now considered a potential mechanism linking metabolic syndrome to depression.
How common: Pre-diabetes affects approximately 2 million Australians, many of whom are undiagnosed. Reactive hypoglycaemia is common but rarely tested for in psychiatry. If your anxiety symptoms consistently occur 2-4 hours after meals (especially high-sugar meals) and are relieved by eating, blood sugar dysregulation should be investigated. A fasting glucose and HbA1c are standard, but a 2-hour glucose tolerance test may be needed to detect reactive hypoglycaemia.
Clinical note: HbA1c measures average blood sugar over 3 months and is more informative than a single fasting glucose. An HbA1c of 39-47 mmol/mol (pre-diabetes) should prompt lifestyle intervention that may also improve mood symptoms. If you are on psychiatric medications that cause weight gain (olanzapine, quetiapine, mirtazapine), regular HbA1c monitoring is essential — these medications significantly increase diabetes risk.
Cortisol and DHEA-S
What it mimics: Cushing's syndrome (excess cortisol) mimics depression, anxiety, cognitive impairment, insomnia, and psychosis. Addison's disease (cortisol deficiency) mimics depression, chronic fatigue, and apathy. Chronic stress with dysregulated cortisol patterns is associated with treatment-resistant depression and anxiety disorders. DHEA-S (a precursor hormone) declines with age and chronic stress, and low levels correlate with depression severity.
The mechanism: Cortisol is the body's primary stress hormone. It directly affects mood, memory, sleep, and appetite through receptors in the hippocampus, amygdala, and prefrontal cortex. Chronically elevated cortisol shrinks the hippocampus (memory and emotional regulation), enlarges the amygdala (fear and anxiety processing), and reduces prefrontal cortex activity (rational thinking and impulse control). This pattern of brain changes is consistently found in both chronic stress and major depressive disorder. DHEA-S partially counterbalances cortisol's neurotoxic effects — the cortisol-to-DHEA-S ratio may be more informative than cortisol alone.
How common: Clinically significant cortisol abnormalities (Cushing's or Addison's) are rare, but subclinical cortisol dysregulation is extremely common in chronic stress, shift work, chronic pain, and sleep disorders. Morning cortisol is best measured as a fasting blood test between 8-9am (levels naturally peak upon waking). If morning cortisol is abnormal, further testing (24-hour urinary cortisol, dexamethasone suppression test, or salivary cortisol curve) may be warranted.
Clinical note: Cortisol testing is not part of a routine depression screen — your GP must specifically request it. It is most useful when depression or anxiety is accompanied by physical symptoms like unexplained weight gain (particularly central/abdominal), thin skin, easy bruising, facial rounding, or muscle weakness. Exogenous steroids (prednisone, hydrocortisone creams, inhaled corticosteroids) can suppress the adrenal axis and cause depressive symptoms upon withdrawal.
Sex Hormones (Oestrogen, Testosterone, Progesterone)
What it mimics: Oestrogen fluctuations are a primary driver of premenstrual dysphoric disorder (PMDD), perimenopausal depression, and postnatal depression. Low testosterone in men is associated with depression, fatigue, irritability, poor concentration, low motivation, and reduced sense of well-being — symptoms often attributed to "midlife crisis" or burnout. Progesterone has anxiolytic properties via its metabolite allopregnanolone, which acts on GABA receptors — progesterone withdrawal contributes to premenstrual anxiety.
The mechanism: Oestrogen is a potent modulator of serotonin, dopamine, and norepinephrine systems. It increases serotonin receptor density, inhibits monoamine oxidase (the enzyme that breaks down mood neurotransmitters), and promotes BDNF production. During perimenopause, oestrogen levels fluctuate wildly before declining, creating a neurochemical rollercoaster that the brain must constantly adapt to. Testosterone influences dopamine pathways involved in motivation, reward, and energy. SHBG (sex hormone binding globulin) binds testosterone and oestradiol, reducing their bioavailability — elevated SHBG can cause symptoms of deficiency even when total hormone levels appear normal.
How common: Perimenopausal women are 2-4 times more likely to develop depression than pre-menopausal women, even with no prior psychiatric history. Testosterone deficiency affects approximately 1 in 200 men under 60 and up to 1 in 5 men over 70. However, "low testosterone clinics" that diagnose and treat based on a single blood test are concerning — testosterone levels fluctuate significantly throughout the day, with illness, with sleep deprivation, and with obesity. Two morning samples at least 4 weeks apart are required for diagnosis.
Clinical note: Hormonal blood tests must be interpreted in clinical context. For menstruating women, oestradiol and progesterone vary dramatically across the menstrual cycle — the blood must be drawn at the correct phase (usually days 2-5 for baseline, or day 21 for progesterone). For men, testosterone must be drawn before 10am (levels decline throughout the day). Always request both total and free testosterone with SHBG. Elevated SHBG (common with liver disease, hyperthyroidism, and oral contraceptive use) reduces bioavailable hormone despite normal total levels.
C-Reactive Protein and Inflammation
What it mimics: Emerging research shows that chronic low-grade inflammation is present in approximately one-third of people with treatment-resistant depression. This "inflammatory depression" subtype is characterised by fatigue, psychomotor slowing, appetite increase, and poor response to conventional antidepressants — symptoms that overlap with sickness behaviour (the lethargy your body produces when fighting infection).
The mechanism: Pro-inflammatory cytokines (IL-6, TNF-alpha, IL-1 beta) cross the blood-brain barrier and activate microglia (the brain's immune cells), producing neuroinflammation. This disrupts serotonin synthesis by shunting tryptophan away from the serotonin pathway and towards the kynurenine pathway (which produces neurotoxic metabolites). Inflammation also reduces BDNF, impairs neuroplasticity, and disrupts the hypothalamic-pituitary-adrenal (HPA) axis. CRP is the most accessible blood marker for systemic inflammation and serves as a proxy for this neuroinflammatory process.
How common: Studies consistently find elevated CRP (above 3 mg/L) in 25-35% of depressed patients compared to 10-15% of non-depressed controls. The CANTOS trial (2017) demonstrated that reducing inflammation with an anti-inflammatory antibody independently reduced depressive symptoms in cardiac patients. While anti-inflammatory treatment for depression is still experimental, identifying the inflammatory subtype through blood testing may help guide treatment selection — some evidence suggests that anti-inflammatory approaches (omega-3 fatty acids, exercise, certain medications) are more effective in this subgroup.
Clinical note: Standard CRP and hs-CRP are different tests. For cardiovascular and neuroinflammation research, hs-CRP (high-sensitivity) is preferred as it detects the subtle chronic inflammation relevant to depression. CRP above 10 mg/L likely indicates acute infection or autoimmune flare and should not be interpreted as "inflammatory depression." The value for mental health assessment is in the 3-10 mg/L range. Other causes of elevated CRP (obesity, smoking, sleep apnoea, autoimmune disease, gum disease) should be considered before attributing it to a depression subtype.
Coeliac Screen (tTG-IgA)
What it mimics: Coeliac disease is associated with depression, anxiety, brain fog, irritability, and fatigue in up to 30% of patients — often before any gastrointestinal symptoms appear. Neurological and psychiatric manifestations can be the presenting feature of coeliac disease, with gut symptoms arriving months or years later (or never). Some patients are diagnosed with depression or anxiety for years before the underlying coeliac disease is identified.
The mechanism: The gut-brain axis is a bidirectional communication system between the gastrointestinal tract and the brain, mediated by the vagus nerve, immune signalling, and microbial metabolites. Coeliac disease triggers chronic immune activation and intestinal inflammation that increases intestinal permeability, allowing bacterial products and inflammatory molecules to enter the bloodstream and reach the brain. Coeliac disease also causes malabsorption of iron, B12, folate, vitamin D, and zinc — each independently linked to mood disorders. The combination of immune activation plus multiple nutritional deficiencies creates a perfect storm for neuropsychiatric symptoms.
How common: Coeliac disease affects approximately 1 in 70 Australians, but 80% remain undiagnosed. Diagnosis takes an average of 11.7 years from symptom onset. CRITICAL: You must be eating gluten for at least 6 weeks before testing — going gluten-free before the blood test will produce a false-negative result. If you have already stopped gluten, discuss a gluten challenge with your doctor before testing.
Clinical note: Total IgA must be tested alongside tTG-IgA because 2-3% of coeliac patients have IgA deficiency, which produces false-negative results. If IgA is low, IgG-based tests (DGP-IgG or tTG-IgG) should be ordered instead. Non-coeliac gluten sensitivity (NCGS) is a separate condition with similar symptoms but negative coeliac serology — it is diagnosed by exclusion and remains controversial. If coeliac is negative but gluten clearly worsens your symptoms, discuss NCGS with a gastroenterologist.
The Mental Health Blood Panel
If you are experiencing anxiety, depression, or mood changes, these are the blood tests that can identify physical contributors. Most are bulk billed under Medicare when ordered by your GP with a clinical indication.
| Test | What It Checks | Cost (Australia) |
|---|---|---|
| TSH + Free T4 | Thyroid function — mimics depression and anxiety | Bulk billed |
| Iron Studies (Ferritin, Iron, TIBC) | Iron stores — anxiety, fatigue, restlessness | Bulk billed |
| Vitamin B12 | B12 deficiency — depression, cognitive decline, psychosis | Bulk billed |
| 25-Hydroxyvitamin D | Vitamin D — seasonal depression, low mood | Bulk billed* |
| Folate (Serum or Red Cell) | Folate — methylation, neurotransmitter production | Bulk billed |
| HbA1c + Fasting Glucose | Blood sugar — anxiety from reactive hypoglycaemia | Bulk billed |
| Full Blood Count | Anaemia, infection, immune system baseline | Bulk billed |
| CRP or hs-CRP | Inflammation — neuroinflammation subtype of depression | Bulk billed |
| Calcium + Magnesium | Electrolytes affecting nerve function and mood | Bulk billed |
| Liver Function (ALT, GGT) | Liver health — fatigue, medication metabolism | Bulk billed |
| Coeliac Screen (tTG-IgA + Total IgA) | Coeliac disease — gut-brain axis, malabsorption | Bulk billed |
| Morning Cortisol | Adrenal function — chronic stress, Cushing's, Addison's | Bulk billed* |
* Vitamin D testing is bulk billed for high-risk groups (osteoporosis, malabsorption, dark skin, limited sun exposure, liver/kidney disease). Cortisol testing is bulk billed when there is a clinical indication. Your GP can determine eligibility.
Research Corner: The Neuroinflammation Frontier
The most significant shift in psychiatric research over the past decade has been the recognition that inflammation plays a causal role in a subset of depression. This is not the same as saying depression is “just inflammation” — it is the recognition that the immune system and the nervous system are deeply interconnected, and that immune dysfunction can produce genuine psychiatric symptoms.
The gut-brain axis is another frontier. The gut contains 95% of the body's serotonin and is home to trillions of bacteria that produce neurotransmitters, vitamins, and signalling molecules. Disruptions to the gut microbiome (from antibiotics, diet, infection, or coeliac disease) can alter brain chemistry through multiple pathways: vagus nerve signalling, immune activation, tryptophan metabolism, and short-chain fatty acid production.
What this means practically: if you have depression with elevated inflammatory markers (CRP above 3 mg/L), digestive symptoms, autoimmune conditions, or treatment resistance to conventional antidepressants, it may be worth discussing the inflammatory and gut-brain dimensions with your treating clinician. Anti-inflammatory strategies (exercise, omega-3 fatty acids, Mediterranean diet, addressing sleep apnoea) have supportive evidence as adjuncts to standard treatment.
Before Starting or Changing Medication
If your GP or psychiatrist is prescribing antidepressant or anti-anxiety medication, baseline blood tests serve several critical purposes:
Rule out physical mimics
Treating hypothyroidism with antidepressants is ineffective and delays the correct treatment. Thyroid, iron, B12, and folate should be checked before assuming the cause is psychiatric.
Establish baseline organ function
Many psychiatric medications are processed by the liver and kidneys. Baseline ALT, GGT, creatinine, and eGFR help identify potential contraindications and provide comparison values for monitoring.
Predict treatment response
Emerging evidence suggests that patients with elevated CRP may respond better to certain antidepressants (nortriptyline) than others (escitalopram). Low folate reduces SSRI effectiveness and may be addressed with supplementation.
Monitor metabolic side effects
Atypical antipsychotics (quetiapine, olanzapine) and some antidepressants (mirtazapine) cause significant weight gain and metabolic changes. Baseline HbA1c, fasting glucose, and lipid panel allow early detection of metabolic syndrome.
What to Ask Your Doctor
Ready-to-use script for your GP appointment:
“I have been experiencing [anxiety / low mood / brain fog / fatigue / mood swings] and I'd like to rule out any physical contributors before we discuss other options. Could we check my thyroid function, iron studies with ferritin, B12 and folate, vitamin D, fasting glucose and HbA1c, and a full blood count? I understand these are generally bulk billed and I'd like to have a complete picture.”
This is a reasonable, evidence-based request. Any GP who dismisses it is not following best-practice guidelines. The RANZCP and NICE (UK) guidelines both recommend these baseline investigations for new presentations of depression and anxiety.
TSH + Free T4 (thyroid)
Iron Studies with Ferritin
Vitamin B12
Folate (serum or red cell)
25-Hydroxyvitamin D
HbA1c + Fasting Glucose
Full Blood Count
CRP (inflammation)
Calcium + Magnesium
Coeliac Screen (tTG-IgA)
Liver Function (ALT, GGT)
Kidney Function (eGFR, Creatinine)
Blood Tests Don't Invalidate Mental Illness
This page is not about proving that mental illness is “really” a physical problem. Depression, anxiety, PTSD, and other psychiatric conditions are real, serious, and valid regardless of what blood tests show. The brain is a physical organ, and all mental experiences — whether caused by thyroid dysfunction or childhood trauma — have a biological substrate.
The purpose of blood testing in mental health is not to minimise or delegitimise psychiatric diagnoses. It is to ensure that treatable physical contributors are not overlooked. Finding that low iron is contributing to your anxiety does not mean your anxiety is not real — it means there is a straightforward intervention that can help.
Many people have both physical and psychological factors contributing to their symptoms. Treating the physical factors (correcting iron, optimising thyroid, supplementing B12) often makes psychological treatments more effective, not less necessary. The goal is comprehensive care, not either/or.
Related Reading
Check Your Mental Health Markers
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SmarterBlood provides health information and AI-powered blood test analysis. It is not a substitute for professional medical advice, diagnosis, or treatment. If you are experiencing a mental health crisis, please contact Lifeline on 13 11 14 or Beyond Blue on 1300 22 4636.