Thyroid Diet: What to Eat for Hypo and Hyperthyroidism

Thyroid diet — at a glance, here are the most important points to walk away with before you read the deep dive below.

• Iodine and selenium are the two most critical thyroid nutrients — two to three Brazil nuts daily covers selenium needs, while iodine comes mainly from dairy, seafood, and eggs. • Goitrogens in cruciferous vegetables are only clinically significant alongside iodine deficiency, and cooking reduces their goitrogenic activity by 30–90 per cent — normal dietary amounts are safe for most people. • Levothyroxine should be taken on an empty stomach, separated by at least four hours from calcium, iron, soy, coffee, and high-fibre foods, all of which impair its absorption. • Selenium supplementation (200mcg daily) has the strongest single-nutrient evidence for reducing TPO antibodies in Hashimoto's thyroiditis. • Hyperthyroidism and Graves' disease call for higher protein and calorie intake to offset accelerated metabolism and bone turnover, and avoidance of excess iodine from seaweed or kelp. • Roughly 90 per cent of hypothyroidism in iodine-sufficient countries is autoimmune, so gut-supportive, anti-inflammatory eating and regular ferritin and vitamin D testing matter as much as thyroid-specific nutrients.

The thyroid gland requires several specific micronutrients to synthesise and convert thyroid hormones. Deficiency in any of these can impair thyroid function, worsen symptoms, and in some cases precipitate thyroid dysfunction.

Iodine is the most critical thyroid nutrient — it is literally incorporated into thyroid hormone molecules (T3 contains three iodine atoms; T4 contains four). Iodine deficiency is the leading preventable cause of hypothyroidism and goitre worldwide, affecting an estimated two billion people. In iodine-sufficient countries like the US, Canada, and Australia, iodine deficiency is less common but still occurs, particularly in women who avoid dairy and seafood. UK iodine status is borderline in many population groups, with recent National Diet and Nutrition Survey data showing concerning deficiency rates in young women and teenagers.

Dietary sources of iodine include dairy milk (a major source in the UK and US due to iodine in cattle feed and cleaning agents), seafood and sea fish, eggs, and iodised salt (used in the US and many other countries but not widely in the UK). Seaweed is an extremely concentrated iodine source — particularly kelp and kombu — and can actually provide dangerously excessive amounts if consumed frequently; more moderate seaweed varieties like nori (used in sushi) are safer. The recommended daily intake for adults is 150 micrograms, rising to 250 micrograms in pregnancy and lactation.

Selenium is essential for the conversion of T4 (the inactive prohormone produced by the thyroid) to T3 (the active hormone), a process that occurs primarily in the liver and kidneys and requires selenoenzymes called deiodinases. Selenium also protects the thyroid gland itself from oxidative damage — the thyroid has the highest selenium concentration of any organ. Multiple trials have shown that selenium supplementation (200 micrograms daily) reduces thyroid peroxidase antibodies (TPO-Ab) in Hashimoto's thyroiditis and may slow disease progression. Just two to three Brazil nuts per day provides sufficient selenium, making this one of the most practical dietary interventions for thyroid health. Avoid selenium supplements above 400 micrograms daily — toxicity (selenosis) causes hair loss, nail changes, and neurological effects.

Goitrogens are compounds found in certain foods that can interfere with thyroid hormone synthesis by inhibiting thyroid peroxidase (the enzyme that incorporates iodine into thyroid hormones) or by competing with iodine uptake. Foods containing goitrogens include cruciferous vegetables (broccoli, kale, cabbage, Brussels sprouts, cauliflower, bok choy), soy foods, millet, cassava, peanuts, and peaches.

The internet is full of alarming advice for hypothyroid patients to eliminate or severely restrict these foods. This advice is largely excessive and potentially counterproductive. The scientific reality is more nuanced: goitrogenic effects from food are only clinically significant in the context of concurrent iodine deficiency. In iodine-sufficient individuals, the quantities of cruciferous vegetables consumed in a normal diet do not meaningfully impair thyroid function. Multiple large population studies have found no association between cruciferous vegetable consumption and thyroid disease incidence.

Furthermore, cooking significantly reduces the goitrogenic activity of cruciferous vegetables. Steaming, boiling, stir-frying, and roasting degrade glucosinolates (the precursors to goitrogens) by 30 to 90 per cent. Raw preparations (raw kale smoothies consumed in large volumes daily) carry more theoretical risk, though even here the evidence of clinical harm in iodine-sufficient people with treated hypothyroidism is limited.

Soy is a more complex case. Soy isoflavones can inhibit thyroid peroxidase and may affect thyroxine absorption when consumed at the same time as levothyroxine medication. The clinical guidance is to separate soy foods from levothyroxine by at least four hours, which adequately addresses the absorption interaction. Moderate soy consumption as part of a varied diet does not cause thyroid dysfunction in iodine-sufficient people without thyroid disease.

Rather than eliminating nutritious foods based on overcautious goitrogen concerns, focus on ensuring adequate iodine intake and separating thyroid medication from potential absorption inhibitors.

Hashimoto's thyroiditis is an autoimmune condition in which the immune system attacks thyroid tissue, leading to progressive hypothyroidism. Dietary strategies for Hashimoto's therefore address both the hypothyroid state and the underlying autoimmune activity.

An anti-inflammatory diet is the foundation. The autoimmune Paleo (AIP) diet — which eliminates grains, legumes, dairy, eggs, nightshades, nuts, seeds, and processed foods — has received attention in the autoimmune community and small pilot studies have shown reductions in Hashimoto's symptoms and some inflammatory markers. However, it is highly restrictive, difficult to sustain, and lacks robust long-term clinical trial evidence. A less restrictive anti-inflammatory Mediterranean approach — rich in fish, vegetables, olive oil, legumes, and wholegrains — provides many of the same anti-inflammatory benefits with greater practicality and nutritional completeness.

Gluten is debated in Hashimoto's. Coeliac disease and Hashimoto's co-occur at higher rates than chance would predict (approximately 5% of Hashimoto's patients have coeliac disease compared to 1% in the general population), and both non-coeliac gluten sensitivity and molecular mimicry (where gluten peptides resemble thyroid tissue, potentially triggering cross-reactive antibodies) have been proposed as mechanisms. Testing for coeliac disease should be a priority for anyone with Hashimoto's. For those who test negative, gluten-free trials may still be worth considering under dietitian guidance, though evidence is not conclusive.

Selenium supplementation (200 micrograms daily from selenomethionine or high-selenium yeast, not sodium selenite) has the strongest single nutrient evidence for Hashimoto's, with multiple meta-analyses showing meaningful reductions in TPO-Ab and improved thyroid ultrasound findings. Vitamin D deficiency is highly prevalent in Hashimoto's and independently associated with antibody levels — optimise vitamin D status. Zinc supports thyroid hormone synthesis and immune regulation; good sources include oysters, pumpkin seeds, beef, and cashews.

Hyperthyroidism involves excessive thyroid hormone production, leading to symptoms including weight loss despite good appetite, rapid heart rate, anxiety, tremors, heat intolerance, and disrupted sleep. Graves' disease (an autoimmune condition where antibodies stimulate the TSH receptor) accounts for the majority of hyperthyroidism in women.

Nutritional priorities differ substantially from hypothyroidism. The elevated metabolic rate driven by excess thyroid hormones increases caloric requirements, protein turnover, and micronutrient needs. Adequate caloric and protein intake is essential to prevent muscle wasting — hyperthyroidism increases protein catabolism. Aim for higher protein intake (1.5–2.0g per kg body weight) and sufficient total calories to maintain body weight.

Calcium and vitamin D are particularly important because hyperthyroidism accelerates bone turnover and bone loss, increasing osteoporosis risk. Dairy, calcium-rich plant foods, and vitamin D supplementation should be prioritised. Adequate calcium intake of at least 1,000–1,200mg daily and vitamin D supplementation to maintain sufficiency is important, particularly for post-menopausal women with hyperthyroidism.

Iodine requires special consideration in hyperthyroidism. Excess iodine can worsen hyperthyroidism by providing additional substrate for excessive thyroid hormone production. High-iodine foods like seaweed, kelp supplements, and very high-dose iodine supplements should be avoided in untreated or poorly controlled hyperthyroidism. Once thyroid function is stabilised with medication or following definitive treatment, dietary iodine from normal food sources is generally fine.

Soy flavonoids may interfere with the thyroid medication carbimazole in some contexts, so moderate soy intake is advisable, particularly around medication times. Stimulants including caffeine, alcohol, and other nervous system stimulants can exacerbate the anxiety, palpitations, and insomnia associated with hyperthyroidism and should be minimised.

Levothyroxine (also known as Synthroid, Eltroxin, or Euthyrox) is the most commonly prescribed thyroid medication, taken by millions of people with hypothyroidism. Its absorption is exquisitely sensitive to dietary factors, and understanding medication-food interactions is essential for ensuring consistent thyroid hormone levels.

Levothyroxine should always be taken on an empty stomach — at least 30 minutes, ideally 60 minutes before breakfast — and with water only. Several foods and supplements dramatically reduce its absorption: calcium (from dairy, antacids, or calcium supplements), iron (from iron-rich foods or supplements), coffee, soy foods, high-fibre foods (particularly bran), and grapefruit all impair absorption if consumed too close to the medication dose. This is not a reason to avoid these foods — it is a reason to separate them from medication timing.

For people who struggle to take medication before breakfast — perhaps because of nausea, early feeding requirements, or simply forgetting — taking levothyroxine at bedtime (at least three to four hours after the last meal) is an evidence-based alternative that improves absorption for many people. Discuss this with your endocrinologist.

Calcium supplements and iron supplements are best taken at least four hours apart from levothyroxine. If you are prescribed both iron and levothyroxine, take levothyroxine first thing in the morning and iron later in the day — not simultaneously. Coffee drinkers who find they struggle to wait before their morning coffee can try taking levothyroxine at bedtime as an alternative.

For people on anti-thyroid medication (carbimazole or propylthiouracil), drug-food interactions are less significant, but consistent iodine intake (neither very high nor fluctuating) supports more stable medication dosing.

Roughly 90 percent of hypothyroidism in iodine-sufficient countries is autoimmune (Hashimoto's), and the gut-immune axis has become a central area of research. Increased intestinal permeability ('leaky gut'), dysbiosis, and chronic low-grade inflammation are commonly observed alongside elevated TPO antibodies. The dietary implication is not exotic — it is the same anti-inflammatory pattern that benefits most autoimmune conditions: abundant fibre from vegetables, legumes and whole grains to feed beneficial bacteria; one or two servings of fermented foods daily (kefir, sauerkraut, kimchi, miso, live yogurt); two to three portions of oily fish per week for omega-3s; and minimal ultra-processed foods, refined sugars and emulsifier-heavy packaged products.

Iron and ferritin status matter more than is widely recognised — sub-optimal ferritin (below ~70 ng/mL) is independently associated with persistent fatigue and hair loss in hypothyroid patients even when TSH is in range, and impaired iron status reduces T4-to-T3 conversion. Women with heavy periods or vegetarian diets should have ferritin tested annually alongside TSH and T4. Building a Mediterranean-aligned pattern such as the [low-FODMAP-friendly anti-inflammatory approach](/blog/low-fodmap-ibs-protocol/) (if IBS-overlap exists) or a broader [Mediterranean foundation](/blog/mediterranean-diet-gold-standard/) handles most of these levers at once. Diet does not replace medication, but it consistently reduces antibody titres in selenium-and-vitamin-D-replete patients across multiple trials.

Stubborn weight gain is the symptom most commonly attributed to hypothyroidism, but the picture is more nuanced. Untreated hypothyroidism reduces basal metabolic rate measurably — typically 10 to 20 percent — and once treatment restores TSH to normal range, BMR largely normalises. The persistent weight that remains tends to reflect months of fluid retention, slowed gut motility, and reduced spontaneous activity during the under-treated period, not an ongoing metabolic curse. Realistic expectations matter: research suggests once euthyroid, weight loss responds to standard energy-deficit principles, though it often feels slower in the first three to six months while body composition and hydration re-stabilise.

Practical levers that work alongside well-titrated medication: prioritise protein (1.2 to 1.6 g/kg/day) to counter the muscle loss that often accompanies under-treated hypothyroidism, walk daily to support NEAT, and address the fatigue-overeating loop by anchoring sleep at seven to eight hours. For hyperthyroidism, the opposite challenge applies — the metabolic surge typically causes unintentional weight loss, and high-quality, calorie-dense whole foods (nuts, olive oil, full-fat dairy, whole grains, oily fish) help maintain weight without resorting to ultra-processed options. Once thyroid status stabilises, both groups respond to standard nutrition principles, with diet quality and protein adequacy doing most of the work.

The guidance in this article draws on peer-reviewed nutrition and food-science literature as well as guidance from major public-health bodies. Key reference sources we have consulted while writing and updating this piece include:

• Harvard T.H. Chan School of Public Health, *The Nutrition Source*, 2024. • U.S. National Institutes of Health (NIH), Office of Dietary Supplements, fact sheets, 2024. • World Health Organization (WHO), Healthy Diet fact sheet, 2024. • Cochrane Database of Systematic Reviews — relevant systematic reviews, 2020–2024. • British Dietetic Association (BDA) Food Fact Sheets, 2024.

These references are provided so that motivated readers can verify claims and explore the underlying evidence directly. Where a specific trial, meta-analysis, or named author is referenced in the body of the article, that citation takes precedence over the general sources listed here. The article is reviewed periodically against newly published evidence and updated when meaningful new findings emerge.