Hashimoto's Anxiety and Depression: Causes and What Helps

Hashimoto's anxiety is real, measurable and frequently treatable. In a 2018 meta-analysis of 19 studies and more than 36,000 participants, people with autoimmune thyroiditis had 2.32 times the odds of an anxiety disorder and roughly 3.3 to 3.6 times the odds of depression compared with controls (Siegmann et al., JAMA Psychiatry, 2018). A 2024 meta-analysis restricted to people with normal thyroid hormone levels still found 2.5 times the odds of anxiety disorders (Wang et al., Comprehensive Psychoneuroendocrinology, 2024). The usual drivers are a thyroid dose that is off, hormone swings from an inflamed gland, nutrient deficiencies and inflammation, and most of them can be checked with a blood test.

This guide covers what the research shows, which mechanisms are proven and which are speculative, how to work out your likely driver, and which treatments have evidence. It is written for people already diagnosed with Hashimoto's thyroiditis who feel anxious, low, irritable or emotionally unstable. Discuss every medication and supplement change with your doctor.

Can Hashimoto's Cause Anxiety? What the Research Shows

The short answer is yes, through several routes. The longer answer is that the size of the link depends on who was studied.

The Siegmann 2018 meta-analysis

Siegmann and colleagues pooled 19 case-control studies (21 samples, 36,174 participants). People with autoimmune thyroiditis, Hashimoto's, or subclinical or overt hypothyroidism had an odds ratio of 2.32 for anxiety disorders and 3.56 for depression. A 2019 correction added an omitted large study and revised the depression estimate to 3.31 (Siegmann & Grömer, JAMA Psychiatry, 2019).

The authors were candid about limits. Heterogeneity was very high (I² around 90%), every study was case-control, and the funnel plot suggested publication bias for depression. They also did not separate euthyroid patients from hypothyroid ones, so the pooled numbers mix antibody effects with hormone effects. Their clinical recommendation was practical: people with depression or anxiety should be tested for thyroid autoimmunity, including TPO antibodies, and people with Hashimoto's should be screened for psychiatric symptoms.

The euthyroid question: does it happen with normal TSH?

This is the question most patients care about. Their labs are "normal," yet they feel anxious.

Wang and colleagues pooled studies of people with Hashimoto's and normal thyroid hormone levels. For anxiety, eight studies (516 patients, 493 controls) gave an odds ratio of 2.52. Beck Anxiety and Beck Depression scores were both higher in the Hashimoto's groups (Wang et al., 2024). An earlier community study in Sardinia found anti-TPO positivity was more common in people with anxiety disorders (OR 4.2) and mood disorders (OR 2.9) (Carta et al., BMC Psychiatry, 2004).

A 2021 systematic review of 30 studies reached a similar conclusion for broader symptoms: most studies found that thyroid autoimmunity was associated with persisting symptoms or lower quality of life in biochemically euthyroid people (Groenewegen et al., Journal of Translational Autoimmunity, 2021).

The studies that found nothing

Honesty requires the other side. The Norwegian HUNT study screened a population of 30,175 adults and found no association between TPO antibodies and anxiety or depression, crude or adjusted (Engum et al., Journal of Psychosomatic Research, 2005). A 2026 meta-analysis of 12 population-based studies (676,658 participants) found a small, non-significant estimate for TPO antibodies and anxiety (OR 1.47, 95% CI 0.73 to 2.94) and called the evidence inconclusive (Ivens et al., 2026).

Population studies are less prone to selection bias than clinic samples, because clinic patients are often the sickest. The likely reading: thyroid autoimmunity raises the risk of anxiety and depression modestly across the population, and much more in the subgroup of patients who are symptomatic enough to seek care.

Why Hashimoto's Affects Mood: Five Mechanisms

Mood symptoms in Hashimoto's rarely have a single cause. These are the drivers with the best support, roughly in order of how often they turn out to matter.

1. Hormone levels that are off (in either direction)

Thyroid hormone sets the pace for brain tissue. Too little produces slowed thinking, flat mood and fatigue. Too much produces restlessness, irritability, insomnia and anxiety. Both states are common in Hashimoto's because the gland's output falls over years, so a dose that was right two years ago can be wrong today.

The overtreated side is under-recognized. A suppressed TSH on levothyroxine can produce palpitations, tremor and a jittery, panicky feeling that looks like an anxiety disorder. Long-term overtreatment also carries real risks, including atrial fibrillation and bone loss in older adults, so this is worth correcting for reasons beyond mood.

2. Hashitoxicosis: the swing pattern

In early or active Hashimoto's, immune attack can rupture thyroid follicles and release stored hormone into the blood. The result is a temporary hyperthyroid phase, often called hashitoxicosis, followed by a drop as the damaged tissue produces less.

Patients often describe this as mood swings: weeks of anxiety, racing heart and poor sleep, then a slide into exhaustion and low mood. Because labs are often drawn only once, the pattern is easy to miss. The same anxious-then-low sequence is typical of postpartum thyroiditis, which is one reason new anxiety in the year after birth deserves thyroid testing. For flare triggers and timing, see the Hashimoto's flare-up guide.

3. T3 in the brain

The brain does not rely only on circulating T3. Glial cells convert T4 into T3 locally through the type 2 deiodinase enzyme, then pass it to neurons. This local conversion is one proposed explanation for why some people on levothyroxine feel unwell with normal blood tests. The brain-specific evidence is covered in depth in the Hashimoto's brain fog article.

The psychiatric field takes the thyroid-mood link seriously in a different way. In the STAR*D trial, adding T3 (up to 50 mcg per day) for treatment-resistant depression produced a 24.7% remission rate versus 15.9% for lithium, a difference that was not statistically significant but came with fewer side effects (Nierenberg et al., American Journal of Psychiatry, 2006). Those patients did not have Hashimoto's. The trial shows that thyroid hormone acts on mood circuits. It says nothing about whether a given Hashimoto's patient needs T3.

4. Inflammation and antibodies

Inflammatory cytokines such as IL-6 and TNF-alpha affect serotonin and dopamine metabolism and are elevated in a subset of people with depression. Hashimoto's is a chronic inflammatory disease, so this is a plausible bridge. The strongest hint that the autoimmune process matters independently of hormone levels comes from a Norwegian trial: 150 euthyroid Hashimoto's patients with persistent symptoms and TPO antibodies above 1,000 IU/mL were randomized to thyroidectomy or continued medical care. Only the surgery group improved, with general health scores rising from 38 to 64 points and chronic fatigue falling from 82% to 35% (Guldvog et al., Annals of Internal Medicine, 2019).

That trial measured quality of life and fatigue, not anxiety or depression specifically, and had no sham control. Read it as a clue about mechanism. Nobody should have thyroid surgery to treat anxiety or depression.

5. Nutrient deficiencies that cause mood symptoms on their own

B12, iron and vitamin D deficiencies all cluster with Hashimoto's, and the first two cause psychiatric symptoms directly.

• B12: Autoimmune gastritis, which destroys the stomach cells needed to absorb B12, occurs more often alongside Hashimoto's. A 2023 meta-analysis of 64 studies found B12 deficiency in about 27% of people with hypothyroidism and 18% with autoimmune thyroid disease (Benites-Zapata et al., Frontiers in Endocrinology, 2023). B12 deficiency can cause depression, irritability, memory problems and numbness.
• Iron: In a Taiwanese national database of adults, iron deficiency anemia was associated with a 52% higher risk of psychiatric disorders, including anxiety and depressive disorders (Lee et al., BMC Psychiatry, 2020). Iron is also needed to make thyroid hormone; see iron deficiency in Hashimoto's.
• Vitamin D: Low levels are common in Hashimoto's, but correcting vitamin D has not been shown to prevent depression (see the treatment section below).

Find Your Likely Driver

Anxiety and depression in Hashimoto's tend to follow recognizable patterns. Use this as a conversation starter with your doctor, not as a diagnosis.

Hashimoto's panic attacks

Panic-like episodes deserve a specific note. A pounding heart, trembling hands, sweating, air hunger and a sense of doom are classic panic symptoms, and they are also classic symptoms of excess thyroid hormone. If episodes began after a dose increase, a brand switch, or alongside weight loss and heat intolerance, ask for TSH and free T4 before assuming panic disorder.

If thyroid levels are normal, panic disorder is one of the most treatable conditions in psychiatry. Panic attacks are not a reason to change your thyroid dose by yourself.

Hashimoto's mood swings and irritability

Irritability is underreported in thyroid disease. It shows up with overtreatment, during hashitoxicosis, with poor sleep, and with B12 deficiency. Tracking mood daily alongside dose changes, menstrual cycle and sleep for four to six weeks often reveals a pattern that a single office visit cannot. In perimenopause, hormone shifts add another layer that overlaps with thyroid symptoms.

Labs to Ask For

Most of these are standard tests your primary care doctor can order. The goal is to rule in or out the fixable causes before attributing everything to "just anxiety" or "just Hashimoto's."

For functional versus standard reference ranges on thyroid markers, ferritin and vitamin D, see Hashimoto's lab targets. For how to read antibody results, see our TPO and Tg antibody guide.

A validated mood screen belongs in the workup too. The PHQ-9 (depression) and GAD-7 (anxiety) take two minutes each and give you and your doctor a baseline to track.

Levothyroxine and Anxiety: The Dose Question

Getting the thyroid dose right is the single most important step, and it has two sides.

When the dose is too low or too high

Correcting overt hypothyroidism improves mood for most people, and correcting overtreatment removes a common cause of anxiety. These are standard endocrinology, Grade A by any measure. Dose requirements change with weight, age, pregnancy, menopause, new medications and the gradual loss of thyroid tissue, so a yearly or symptom-triggered recheck is reasonable.

Practical points that affect your levels:

• Take levothyroxine consistently, on an empty stomach, apart from iron, calcium, coffee and soy.
• Blood should be drawn before your morning dose for consistent free T4 readings.
• After any dose or brand change, levels take about 6 weeks to settle. Recheck at 6 to 8 weeks.

When the TSH is already in range

Here the evidence is sobering. In a double-blind trial, 138 people on levothyroxine with normal TSH were randomized to keep their dose, raise it or lower it, targeting TSH ranges of roughly 0.34 to 2.5, 2.5 to 5.6, or 5.6 to 12 mU/L. After six months there were no meaningful differences in quality of life, mood or cognition. Participants could not tell which way their dose had moved, yet they preferred the dose they believed was higher (Samuels et al., Journal of Clinical Endocrinology and Metabolism, 2018).

In-range symptoms are still real. Pushing the dose higher within the normal range rarely fixes mood on its own, and it can tip people into overtreatment and anxiety. When TSH is in range and mood remains poor, the next step is to look elsewhere: nutrients, sleep, inflammation, and direct treatment of the anxiety or depression. Options such as combination T4 plus T3 therapy are covered in our levothyroxine alternatives guide.

What Helps: Evidence-Graded Treatments

Grades follow our standard scale. Grade A: multiple RCTs or meta-analyses. Grade B: a single RCT, case series, or strong mechanistic plus clinical evidence. Grade C: preliminary or mechanistic evidence only. Where a treatment is proven for anxiety or depression in general but untested in Hashimoto's specifically, we say so.

Optimize thyroid replacement [Grade A for correcting true under- or overtreatment]

Covered above. Fix clear dosing problems first. Avoid chasing small TSH changes for mood alone.

Psychotherapy, including CBT [Grade A for anxiety and depression generally; Grade C in Hashimoto's specifically]

Cognitive behavioral therapy is a first-line treatment for generalized anxiety, panic disorder and depression, with decades of RCT support. Hashimoto's-specific trials are scarce. In one 2025 RCT, 70 adults with Hashimoto's who added ten group sessions of a trauma-focused therapy to usual care improved on depression, anxiety and stress at follow-up compared with usual care alone (Macarenco et al., European Journal of Psychotraumatology, 2025). A reported drop in TPO antibodies did not hold up in the complete-case analysis, and dropout in the control group was high, so treat it as preliminary.

Therapy works on the anxiety itself, whatever started it. Health anxiety, which is common after any chronic diagnosis, responds especially well to CBT.

Exercise [Grade A for depression generally]

A 2024 network meta-analysis of 218 RCTs (14,170 participants with major depression) found moderate reductions in depression from walking or jogging, yoga, strength training, mixed aerobic exercise and tai chi, with larger effects at higher intensity (Noetel et al., BMJ, 2024). Confidence in the evidence was rated low to very low because few trials could blind participants, but the direction was consistent. In Hashimoto's, the main caveat is recovery: very long or intense sessions can leave some patients depleted. The Hashimoto's exercise guide explains how to dose it.

Antidepressants and anti-anxiety medication [Grade A for depression and anxiety disorders]

SSRIs and SNRIs are compatible with levothyroxine and are commonly prescribed together. Siegmann and colleagues suggested early antidepressant treatment in patients with thyroid autoimmunity and mood symptoms, and preferred SSRIs over older tricyclics in hypothyroid patients.

Practical safety points:

• Tell both prescribers about all your medications. Ask whether a TSH recheck 6 to 8 weeks after starting or changing an antidepressant makes sense for you.
• Lithium, used for bipolar disorder, can cause hypothyroidism and needs regular thyroid monitoring. Your prescriber should already be doing this.
• Never stop or taper a psychiatric medication on your own because you have found a thyroid explanation. Abrupt discontinuation can cause withdrawal symptoms and relapse. Both problems can be present at once.

T3 augmentation [Grade B, prescriber-led only]

In treatment-resistant depression, psychiatrists sometimes add T3 to an antidepressant, based on STAR*D and earlier trials. This is a psychiatric decision made with monitoring, distinct from thyroid replacement. Do not add T3 yourself; excess T3 causes anxiety, palpitations and arrhythmia risk.

Correct B12 deficiency [Grade B when deficient]

If B12 or methylmalonic acid confirms deficiency, treatment with oral high-dose B12 or injections reverses many neuropsychiatric symptoms over weeks to months, depending on duration and severity. Without a deficiency, extra B12 is not an antidepressant. If autoimmune gastritis is suspected, your doctor may test for intrinsic factor or parietal cell antibodies.

Correct iron deficiency [Grade B when deficient]

Iron repletion improves fatigue and is needed for thyroid hormone synthesis. The mood evidence is mostly observational; in the Taiwanese database, people with iron deficiency anemia who received iron treatment had lower psychiatric risk than those who did not (Lee et al., 2020). Supplement only when labs confirm a need, and take iron at least four hours apart from levothyroxine.

Selenium [Grade A for lowering TPO antibodies; Grade C for mood]

Selenium (typically 200 mcg selenomethionine) lowers TPO antibodies in many trials; the details and caveats are in our selenium for Hashimoto's guide. For mood, the evidence is thin. In a 2026 pilot study of 78 reproductive-age women with euthyroid Hashimoto's, six months of selenomethionine lowered Beck Depression scores only in the group with adequate vitamin E intake (Krysiak et al., Antioxidants, 2026). There was no placebo group. Keep total selenium at or below 400 mcg per day from all sources.

Vitamin D [Grade C for mood]

Correct a deficiency for bone, immune and thyroid reasons; see vitamin D and the thyroid. For depression, the largest trial is clear. VITAL-DEP randomized 18,353 adults aged 50 and older to 2,000 IU of vitamin D3 daily or placebo for a median 5.3 years and found no reduction in depression risk (HR 0.97) or change in mood scores (Okereke et al., JAMA, 2020). Fix a vitamin D deficiency for its own sake and expect little change in mood.

Sleep and stress load [Grade B]

Poor sleep amplifies both anxiety and thyroid symptoms. Cortisol, the HPA axis and stress-reduction methods such as MBSR and yoga are covered in Hashimoto's and stress, so they are not repeated here. If you are considering ashwagandha for anxiety, read ashwagandha and the thyroid first: it can raise thyroid hormone levels, which is a problem if you are already on levothyroxine or prone to hashitoxicosis.

How Hashimoto's Mood Symptoms Overlap with Fatigue and Brain Fog

Depression, Hashimoto's fatigue and brain fog share symptoms: low energy, poor concentration, loss of interest and slowed thinking. They also share causes. A useful distinction is that depression usually includes low mood or loss of pleasure for most of the day, while fatigue alone can coexist with normal mood and interest.

Telling them apart matters because the treatments differ. Fatigue from low ferritin improves with iron. Depression improves with therapy or medication. Brain fog from undertreatment improves with dose correction. Many patients have more than one, and treating one often helps the others.

Hashimoto's Encephalopathy (SREAT): Rare Red Flags

Hashimoto's encephalopathy, also called steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), is a rare brain disorder. A prospective Italian hospital study estimated its prevalence at about 2.1 per 100,000 (Ferracci et al., Journal of the Neurological Sciences, 2004). It is a diagnosis of exclusion.

Expert criteria published in The Lancet Neurology require all six of the following: encephalopathy with seizures, myoclonus, hallucinations or stroke-like episodes; subclinical or mild overt thyroid disease; a normal or non-specific brain MRI; thyroid antibodies in the blood; absence of well-characterized neuronal antibodies; and reasonable exclusion of other causes (Graus et al., Lancet Neurology, 2016). The same paper notes that thyroid antibodies are present in up to 13% of healthy people, so a positive TPO test cannot diagnose encephalopathy on its own.

Ordinary anxiety, low mood and brain fog are not early encephalopathy. Knowing the red flags lets you act fast in the rare case they appear.

A Practical Plan

1. Safety first. If you have thoughts of self-harm, call or text 988 (US) now. Outside the US, contact your local emergency number or crisis line. If you have red-flag neurological symptoms, go to emergency care.
2. Screen your mood. Complete a PHQ-9 and GAD-7 and bring the scores to your appointment.
3. Check the fixable causes. TSH, free T4, free T3, B12 with MMA, ferritin and iron panel, vitamin D, CBC.
4. Fix clear thyroid dosing problems with your doctor, then recheck at 6 to 8 weeks.
5. Replete confirmed deficiencies. B12, iron and vitamin D only when labs show a need.
6. Start direct mood treatment in parallel. CBT or another evidence-based therapy, regular exercise, and medication if your clinician recommends it. Waiting for thyroid labs to be perfect before treating depression is not necessary.
7. Track for six weeks. Daily mood, sleep, dose, cycle and symptoms.

For the wider plan, including diet, gut health and antibody reduction, see our evidence-based Hashimoto's protocol. To get a protocol matched to your condition, labs and severity, take the free 3-minute quiz.

Frequently Asked Questions

Can Hashimoto's cause anxiety?

Yes. The most common thyroid causes are a levothyroxine dose that is too high and hashitoxicosis, where the inflamed gland releases stored hormone. Meta-analyses find about 2.3 to 2.5 times the odds of anxiety disorders in thyroid autoimmunity, including in people with normal thyroid levels. A separate anxiety disorder can coexist and deserves its own treatment.

Can thyroid antibodies cause anxiety with normal TSH?

Possibly. Clinic-based studies say yes; large population studies are mixed. Antibodies may contribute through inflammation, but they do not explain every case. Check B12, iron and your dose, and treat the anxiety directly.

Are Hashimoto's panic attacks different from regular panic attacks?

They can feel identical. Panic-like symptoms caused by excess thyroid hormone usually come with other signs: weight loss, heat intolerance, tremor, frequent bowel movements, and a low TSH. If labs are normal, standard panic treatment works.

Will treating my thyroid cure my depression?

Sometimes, if your thyroid was clearly undertreated. Often it helps but does not resolve depression completely. Treat both.

Can I take SSRIs with levothyroxine?

Yes. They are commonly used together. Tell both prescribers and ask about a TSH recheck after starting.

Should I stop my antidepressant if my thyroid is the cause?

No. Never stop a psychiatric medication without your prescriber. Thyroid problems and depression often coexist, and stopping abruptly risks withdrawal and relapse.

The Bottom Line

Anxiety and depression are among the most common and least discussed parts of Hashimoto's. Pooled studies show a two- to three-fold higher risk, with the strongest link in people who seek care for symptoms. The most fixable drivers are a thyroid dose that is off, hormone swings from an inflamed gland, and B12 or iron deficiency.

The treatments with Grade A evidence are thyroid dose correction when it is clearly wrong, psychotherapy, exercise and antidepressants. Selenium and vitamin D support the thyroid but are not mood treatments. Fine-tuning a normal TSH rarely changes mood and can cause anxiety. Any sudden confusion, seizures or hallucinations need emergency care.

Find out which interventions fit your condition and labs: take the free AutoimmuneFinder quiz.

This site provides educational information only. Not medical advice. Always consult your healthcare provider before changing your treatment plan. If you are in crisis, call or text 988 (US). Outside the US, contact your local emergency number or crisis line.

References

1. Siegmann EM, Müller HHO, Luecke C, et al. Association of Depression and Anxiety Disorders With Autoimmune Thyroiditis: A Systematic Review and Meta-analysis. JAMA Psychiatry. 2018;75(6):577-584. PMC6137529
2. Siegmann EM, Grömer TW. Additional Data From Omitted Study in a Meta-analysis. JAMA Psychiatry. 2019. PMC6584887
3. Wang B, Huang J, Chen L. Association between depression and anxiety disorders with euthyroid Hashimoto's thyroiditis: a systematic review and meta-analysis. Comprehensive Psychoneuroendocrinology. 2024. PMC11665666
4. Carta MG, Loviselli A, Hardoy MC, et al. The link between thyroid autoimmunity (antithyroid peroxidase autoantibodies) with anxiety and mood disorders in the community. BMC Psychiatry. 2004;4:25. PMC516779
5. Groenewegen KL, Mooij CF, van Trotsenburg ASP. Persisting symptoms in patients with Hashimoto's disease despite normal thyroid hormone levels: does thyroid autoimmunity play a role? Journal of Translational Autoimmunity. 2021. PMC8122172
6. Engum A, Bjøro T, Mykletun A, Dahl AA. Thyroid autoimmunity, depression and anxiety; are there any connections? Journal of Psychosomatic Research. 2005. PubMed 16253615
7. Ivens B, Bode H, Bschor T, Henssler J, Baethge C. Thyroid disorders, thyroid autoimmunity, and anxiety: a systematic review and meta-analysis of population-based studies. 2026. PMC13450037
8. Nierenberg AA, Fava M, Trivedi MH, et al. A Comparison of Lithium and T3 Augmentation Following Two Failed Medication Treatments for Depression: A STAR*D Report. American Journal of Psychiatry. 2006;163(9):1519-1530. Journal
9. Guldvog I, Reitsma LC, Johnsen L, et al. Thyroidectomy Versus Medical Management for Euthyroid Patients With Hashimoto Disease and Persisting Symptoms: A Randomized Trial. Annals of Internal Medicine. 2019. PubMed 30856652
10. Benites-Zapata VA, et al. Vitamin B12 levels in thyroid disorders: a systematic review and meta-analysis. Frontiers in Endocrinology. 2023. PMC9994182
11. Lee HS, Chao HH, Huang WT, et al. Psychiatric disorders risk in patients with iron deficiency anemia and association with iron supplementation medications. BMC Psychiatry. 2020. PMC7216322
12. Samuels MH, Kolobova I, Niederhausen M, et al. Effects of Altering Levothyroxine Doses on Quality of Life, Mood, and Cognition in L-T4 Treated Subjects. Journal of Clinical Endocrinology and Metabolism. 2018. PMC6457033
13. Macarenco MM, Opariuc-Dan C, Georgescu T. The influence of identity-oriented psychotrauma therapy on Hashimoto disease activity: a randomised controlled trial. European Journal of Psychotraumatology. 2025. PMC12203709
14. Noetel M, Sanders T, Gallardo-Gómez D, et al. Effect of exercise for depression: systematic review and network meta-analysis of randomised controlled trials. BMJ. 2024. PMC10870815
15. Krysiak R, Kowalcze K, Ott J, et al. Vitamin E Intake Modulates the Effect of Selenomethionine on Sexual Function and Depressive Symptoms in Reproductive-Age Women with Euthyroid Autoimmune Thyroiditis: A Pilot Study. Antioxidants. 2026. PMC13203289
16. Okereke OI, Reynolds CF, Mischoulon D, et al. Effect of Long-term Vitamin D3 Supplementation vs Placebo on Risk of Depression or Clinically Relevant Depressive Symptoms and on Change in Mood Scores: A Randomized Clinical Trial. JAMA. 2020. Journal
17. Ferracci F, Bertiato G, Moretto G. Hashimoto's encephalopathy: epidemiologic data and pathogenetic considerations. Journal of the Neurological Sciences. 2004. PubMed 14706219
18. Graus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurology. 2016. PMC5066574