Hypothyroidism

Hypothyroidism means that your body has too little thyroid hormone for its needs. It commonly develops gradually and can cause fatigue, cold intolerance, constipation, dry skin, weight change, low mood and slowed thinking. Diagnosis depends on thyroid blood tests, while treatment usually replaces the missing hormone with carefully monitored levothyroxine.

What hypothyroidism is Hypothyroidism is a condition in which thyroid hormone action is insufficient for your body's needs. It is often called an underactive thyroid. The problem may begin in the thyroid gland itself or, less commonly, in the pituitary or hypothalamus that controls it. Thyroid hormones influence energy use, temperature regulation, heart function, digestion, skin, muscles, cognition, fertility and many other processes. Symptoms usually develop gradually and overlap with many common conditions. A diagnosis cannot be made from tiredness or weight gain alone. With appropriate treatment and monitoring, most people can live normally and avoid the complications of prolonged hormone deficiency. Where the thyroid gland is The thyroid is a small gland at the lower front of your neck, below the voice box. It has two lobes joined by a narrow bridge of tissue. The gland lies close to the windpipe and moves during swallowing. A healthy thyroid is usually difficult to see or feel. Thyroid enlargement is called a goitre. A goitre can occur with low, normal or high thyroid function. A neck lump does not prove hypothyroidism. Rapid growth, hoarseness, swallowing difficulty or breathing difficulty needs specific assessment. The thyroid's position makes it accessible to examination, ultrasound and surgery, but blood tests are more important for assessing hormone function. The thyroid hormones T4 and T3 The thyroid produces mainly thyroxine, usually called T4, and a smaller amount of triiodothyronine, called T3. T4 acts largely as a circulating reservoir. Body tissues convert some T4 into the more active T3 according to local needs. T3 binds to receptors within cells and changes the expression of genes involved in metabolism and organ function. A routine diagnosis of hypothyroidism relies mainly on thyroid stimulating hormone and free T4 rather than a T3 measurement. T3 can remain within the reference range until relatively late in primary hypothyroidism, so a normal T3 does not reliably exclude the condition. The hypothalamus and pituitary The thyroid is controlled by structures within the brain. The hypothalamus releases thyrotropin releasing hormone, which signals the pituitary gland. The pituitary then releases thyroid stimulating hormone, usually shortened to TSH. TSH travels through the blood and stimulates the thyroid to make and release T4 and T3. This control system is sometimes called the hypothalamic pituitary thyroid axis. Problems at different levels of this axis produce different blood test patterns and require different monitoring strategies. The TSH and T4 feedback loop The pituitary continuously senses circulating thyroid hormone. When free T4 falls, the pituitary usually releases more TSH. The higher TSH asks a healthy thyroid to increase hormone production. When free T4 rises, TSH production falls. This is a negative feedback loop. It helps keep thyroid hormone within a narrow physiological range. In primary hypothyroidism, the thyroid cannot respond adequately, so TSH rises while free T4 eventually falls. The feedback loop explains why TSH is a sensitive first line test when the pituitary is functioning normally. What free T4 means Most T4 in your blood is attached to carrier proteins. Only a small unbound fraction is biologically available to tissues. A free T4 test estimates this unbound fraction. It is commonly abbreviated to FT4. Changes in pregnancy, illness, medicines and carrier proteins can complicate interpretation of total thyroid hormone measurements. FT4 is interpreted with TSH rather than as an isolated result. Laboratory reference ranges vary, so results should be read using the range reported by the testing laboratory. Primary hypothyroidism Primary hypothyroidism arises from a problem within the thyroid gland. It is by far the most common form. The usual overt pattern is a raised TSH with a free T4 below the reference range. The pituitary is responding appropriately by sending a stronger signal, but the thyroid cannot produce enough hormone. Causes include autoimmune thyroiditis, thyroid surgery, radioiodine treatment, iodine deficiency and some medicines. TSH is generally used to adjust levothyroxine treatment in primary hypothyroidism once the diagnosis is established. Secondary or central hypothyroidism Secondary hypothyroidism results from pituitary disease. Hypothalamic disease can cause a similar pattern and is sometimes included under central hypothyroidism. The pituitary does not provide an appropriate TSH signal despite inadequate thyroid hormone. Free T4 is low, while TSH may be low, normal or only slightly raised. A normal TSH therefore does not exclude central hypothyroidism. Possible causes include pituitary tumours, surgery, radiotherapy, inflammation, head injury and postpartum pituitary damage. Central hypothyroidism requires specialist assessment because other pituitary hormones, including cortisol regulation, may also be affected. Why adrenal function matters in pituitary disease The pituitary also controls cortisol production through adrenocorticotropic hormone. A pituitary disorder can therefore cause both central hypothyroidism and adrenal insufficiency. Starting thyroid hormone can increase metabolic demand and cortisol clearance. In untreated adrenal insufficiency, this can precipitate an adrenal crisis. Clinicians assess possible cortisol deficiency before or alongside treatment when central hypothyroidism is suspected. Symptoms such as severe weakness, low blood pressure, low sodium or hypoglycaemia increase concern but are not diagnostic alone. This is one reason central hypothyroidism should not be managed by adjusting levothyroxine solely according to TSH. Overt hypothyroidism Overt primary hypothyroidism usually means that TSH is above the reference range and free T4 is low. The term overt refers to the biochemical pattern, not necessarily dramatic symptoms. Some people have few complaints despite clearly abnormal tests. Others experience marked symptoms at less extreme hormone abnormalities. Symptom severity and blood test severity do not always match. Treatment is usually indicated because hormone production is insufficient and complications can develop over time. The cause, age, cardiac health and duration of deficiency influence the starting dose and speed of correction. Subclinical hypothyroidism Subclinical hypothyroidism means that TSH is above the reference range while free T4 remains within the reference range. The word subclinical can be misleading because some people have symptoms. It describes the blood test pattern rather than the absence of symptoms. A mildly raised TSH can be temporary. Recovery from illness, laboratory variation, medicines, obesity and early autoimmune disease can contribute. NICE recommends confirming persistent subclinical hypothyroidism with two abnormal TSH results around three months apart before many treatment decisions. The likelihood of progression is greater when TSH is persistently higher, thyroid antibodies are present or there has been thyroid surgery or radioiodine treatment. Hashimoto's thyroiditis In the UK, Hashimoto's disease is the main cause of primary hypothyroidism. It is also called chronic autoimmune thyroiditis. The immune system mistakenly targets proteins within thyroid cells. Inflammation and gradual tissue loss reduce the gland's ability to produce hormone. Thyroid peroxidase antibodies are commonly present. They support an autoimmune cause but do not measure symptom severity. The thyroid may be enlarged early and become smaller later. Some people never notice a change in neck size. Autoimmune thyroid disease can occur alongside type 1 diabetes, coeliac disease, pernicious anaemia and other autoimmune conditions. Thyroid peroxidase antibodies Thyroid peroxidase is an enzyme used during thyroid hormone production. Autoantibodies against it are called TPO antibodies. NICE advises considering one TPO antibody measurement in adults with a raised TSH. A positive result supports autoimmune thyroid disease and increases the likelihood that subclinical hypothyroidism will persist or progress. The antibody level does not determine the levothyroxine dose and usually does not need repeating. A negative result does not exclude every form of autoimmune thyroiditis or another cause of hypothyroidism. Iodine and thyroid hormone Iodine is an essential component of T4 and T3. The thyroid concentrates iodine from the blood to make these hormones. Iodine deficiency remains an important global cause of hypothyroidism, goitre and preventable developmental harm. Severe deficiency is uncommon in the UK, but intake can be low in some people with restrictive diets or without iodine containing foods. Too much iodine can also disrupt thyroid function, particularly in a susceptible thyroid gland. Iodine supplements and seaweed products should not be taken in high doses to treat suspected hypothyroidism without clinical advice. Thyroid surgery Removing the entire thyroid causes permanent hypothyroidism because no functioning gland remains. Lifelong levothyroxine is then required. After removal of one lobe, the remaining tissue may produce enough hormone, but hypothyroidism can develop later. TSH and free T4 are monitored after surgery according to the extent of surgery and the underlying disease. Surgery may have been performed for cancer, nodules, compression or hyperthyroidism. These contexts can alter the target and follow up plan. People treated for thyroid cancer may intentionally receive doses that suppress TSH under specialist supervision, which differs from routine hypothyroidism care. Radioiodine treatment Radioactive iodine is used to treat some forms of hyperthyroidism. Thyroid cells absorb the iodine and are gradually damaged. Hypothyroidism can develop within months or years and may be an expected outcome of definitive treatment. Regular thyroid testing after radioiodine identifies the change before symptoms become severe. Once hypothyroidism develops, levothyroxine replaces the hormone that the treated gland can no longer produce. Previous radioiodine treatment is also relevant when deciding whether persistent subclinical hypothyroidism is likely to represent permanent thyroid disease. Thyroiditis Thyroiditis means inflammation of the thyroid gland. Some forms release stored hormone first, causing a temporary hyperthyroid phase. As stored hormone becomes depleted, a hypothyroid phase can follow. Recovery may occur, or hypothyroidism may become permanent. Postpartum thyroiditis occurs during the year after pregnancy and is often autoimmune. Subacute thyroiditis can cause a painful tender thyroid, fever and a raised inflammatory response. Treatment and monitoring depend on the type of thyroiditis, symptoms and whether thyroid function recovers. Amiodarone Amiodarone is an anti arrhythmic medicine containing a large amount of iodine. It can cause either hypothyroidism or hyperthyroidism. Risk is higher in people with underlying autoimmune thyroid disease, but dysfunction can occur without a previous diagnosis. Thyroid function is checked before treatment, during long term therapy and for a period after amiodarone ends. Amiodarone should not be stopped independently because it may be controlling a dangerous heart rhythm. Endocrine and cardiology input may be needed to treat thyroid dysfunction while preserving essential rhythm treatment. Lithium Lithium can interfere with thyroid hormone release and increase the risk of goitre and hypothyroidism. It is used for bipolar disorder and can be highly effective for mood stabilisation. Thyroid function is monitored during treatment. Hypothyroidism can often be treated with levothyroxine while lithium continues. Stopping lithium suddenly can destabilise mental health and should never be done solely because TSH has risen without specialist review. Kidney function, calcium and lithium levels are also monitored because lithium affects several body systems. Other medicine related causes Some immune treatments and cancer therapies can cause thyroiditis or permanent hypothyroidism. Tyrosine kinase inhibitors, immune checkpoint inhibitors and interferon treatments are examples in specialist practice. Carbamazepine and some other enzyme inducing medicines can increase thyroid hormone metabolism and alter replacement requirements. Excess antithyroid medication used for hyperthyroidism can also produce hypothyroidism. A complete medication history includes prescribed medicines, supplements and recent treatments rather than focusing only on current tablets. Congenital hypothyroidism Some babies are born without a functioning thyroid or with a gland that cannot produce enough hormone. Untreated congenital hypothyroidism can severely affect growth and brain development. Newborn blood spot screening identifies most affected babies before symptoms become apparent. Prompt levothyroxine treatment allows normal development in most cases. This lesson focuses on acquired adult hypothyroidism, but congenital disease shows why thyroid hormone is particularly important for the developing brain. Symptoms develop gradually Hypothyroidism often progresses slowly over months or years. Early symptoms can be subtle and non specific. You may adapt to reduced energy or assume that changes reflect ageing, stress, work or menopause. No single symptom confirms the diagnosis. NICE notes that one symptom alone may not indicate thyroid disease. The probability increases when several compatible symptoms occur together or risk factors are present. Blood testing remains necessary because symptoms overlap with many common physical and psychological conditions. Fatigue and reduced energy Fatigue is one of the most commonly reported symptoms. You may feel physically slowed, sleepy or unable to recover normally after activity. Severe hypothyroidism can reduce exercise tolerance and make everyday tasks feel unusually demanding. Fatigue is also caused by anaemia, sleep disorders, infection, chronic disease, medicines, depression and many other conditions. A normal thyroid test should prompt consideration of these alternatives rather than repeated levothyroxine treatment. When hypothyroidism is confirmed, improvement in energy can take weeks or months after hormone levels normalise. Weight change Hypothyroidism can cause modest weight gain through reduced energy use and retention of salt and water. Large or rapidly progressive weight gain is unlikely to be explained by mild thyroid dysfunction alone. Appetite may remain normal or fall. Weight response to levothyroxine varies and is not the main measure of treatment success. Excess levothyroxine should never be used as a weight loss medicine. It can cause dangerous heart and bone complications. Weight management should consider sleep, medicines, activity, food access and other metabolic conditions alongside thyroid treatment. Cold intolerance Thyroid hormone supports heat production. Low hormone activity can make you feel unusually cold compared with people around you. Hands and feet may feel persistently cool, and cold environments may become harder to tolerate. Cold intolerance also occurs with low body weight, anaemia, poor circulation and other conditions. It is a useful clue when combined with constipation, dry skin, bradycardia or other compatible features. Sudden hypothermia with confusion is not an ordinary chronic symptom and requires emergency assessment. Constipation Reduced thyroid hormone can slow intestinal movement and contribute to constipation. Stools may become less frequent, harder or more difficult to pass. Diet, fluid intake, physical activity and medicines such as opioids or iron can also contribute. Persistent constipation with bleeding, weight loss, vomiting or abdominal swelling requires separate assessment. Levothyroxine may improve thyroid related constipation, but additional bowel management can still be needed. Skin, hair and nails Skin can become dry, cool, rough or pale. Sweating may decrease. Hair can become coarse, dry or diffusely thin, including thinning of the outer eyebrows in more marked disease. Nails may become brittle and grow slowly. Hair loss can temporarily continue after treatment begins because hair growth cycles respond slowly. Iron deficiency, menopause, skin disease, stress and many other causes of hair loss should remain open when thyroid tests are normal. Facial and tissue changes Severe prolonged hypothyroidism can cause puffiness around the eyes and non pitting swelling of the skin. The term myxoedema describes tissue changes caused by accumulation of water binding substances. The voice may become deeper or hoarse, and the tongue may enlarge in severe disease. These features are now uncommon because blood testing usually identifies hypothyroidism earlier. New neck swelling or persistent hoarseness requires direct assessment rather than being assumed to be a hormone symptom. Muscle and joint symptoms Hypothyroidism can cause muscle aching, cramps, stiffness and weakness. Creatine kinase may rise when muscle involvement is substantial. Carpal tunnel syndrome can occur because tissue swelling compresses the median nerve at the wrist. Joint pain can coexist, but hypothyroidism does not explain persistent inflammatory synovitis. Progressive objective weakness, dark urine or severe muscle pain requires assessment for muscle disease or medicine toxicity. Slowed cognition You may notice slower thinking, reduced concentration, forgetfulness or difficulty finding words. These symptoms can resemble depression, sleep deprivation, menopause related cognitive change or medication effects. Severe untreated hypothyroidism can cause marked cognitive impairment, particularly in older adults. Correction may improve cognition, but not every memory symptom resolves if another condition is present. Sudden fluctuating confusion is more consistent with delirium and requires urgent assessment for an acute cause. Low mood and emotional change Hypothyroidism can contribute to low mood, reduced motivation and emotional slowing. Depression can produce similar fatigue, cognitive difficulty, sleep change and weight change. The conditions can coexist. Treating hypothyroidism does not remove the need to assess severe depression or self harm risk. NICE advises considering thyroid testing in adults with depression or unexplained anxiety. Persistent mood symptoms after TSH normalises deserve a broader mental health and physical health review. Menstrual and fertility changes Hypothyroidism can cause heavy, irregular or less frequent periods. Ovulation and fertility can be affected, especially when hormone deficiency is substantial. Raised prolactin can occur because altered hypothalamic signalling stimulates prolactin release. Menstrual change also occurs with pregnancy, polycystic ovary syndrome, perimenopause and many other conditions. Anyone planning pregnancy should have established hypothyroidism optimised because thyroid hormone needs increase early in pregnancy. Sexual and reproductive symptoms in men Men can experience reduced libido, erectile difficulties, reduced fertility or changes in testosterone regulation. These symptoms have many cardiovascular, psychological, medicine related and endocrine causes. Thyroid testing contributes to assessment when other features suggest thyroid dysfunction. Levothyroxine may improve symptoms caused by hormone deficiency but is not a general treatment for sexual dysfunction. Persistent symptoms require evaluation of the broader clinical picture. Heart and circulation effects Hypothyroidism can slow the heart rate and reduce the strength of contraction. It can increase systemic vascular resistance and contribute to a higher diastolic blood pressure. Cholesterol can rise, particularly low density lipoprotein cholesterol. Severe disease can cause fluid around the heart or worsen heart failure, although these complications are uncommon with early treatment. Chest pain, collapse, severe breathlessness or a new rhythm disturbance requires urgent assessment and should not be managed by adjusting thyroid tablets independently. Nerve and balance symptoms Prolonged hypothyroidism can contribute to peripheral neuropathy, altered reflexes and balance difficulty. Tendon reflex relaxation can become slow on clinical examination. Carpal tunnel syndrome may cause numbness or tingling in the thumb, index and middle fingers. Focal weakness, one sided sensory loss or sudden gait change is not a typical uncomplicated presentation. Neurological symptoms require examination because stroke, nerve compression and other disorders can coexist. Overlap with menopause Perimenopause and hypothyroidism can both cause fatigue, low mood, sleep disturbance, weight change, hair change and cognitive complaints. Menopause more characteristically causes hot flushes, night sweats and changing menstrual patterns, but symptoms vary. NICE specifically warns that thyroid dysfunction symptoms may be mistaken for menopause. A thyroid blood test can clarify hormone function when the pattern or risk factors justify testing. A normal TSH should prevent thyroid treatment from being used as a substitute for appropriate menopause assessment. Overlap with anaemia Anaemia can cause tiredness, breathlessness, palpitations, reduced concentration and cold sensitivity. Iron deficiency may also cause hair loss and restless legs symptoms. A full blood count and iron assessment may be appropriate when what the person describes suggests blood loss, poor intake or malabsorption. Heavy menstrual bleeding can contribute to iron deficiency and may itself be influenced by hypothyroidism. Finding one condition should not prevent treatment of the other when both are present. Overlap with chronic fatigue and sleep disorders Fatigue can arise from obstructive sleep apnoea, insomnia, post viral illness, ME/CFS and many chronic diseases. Loud snoring, witnessed breathing pauses and severe daytime sleepiness suggest sleep apnoea. Post exertional malaise requires assessment for ME/CFS rather than escalating levothyroxine when TSH is normal. A normal thyroid result is clinically useful because it redirects assessment towards other causes. Persistent symptoms should not be dismissed simply because hypothyroidism has been excluded. When thyroid tests are appropriate Thyroid testing is appropriate when there is clinical suspicion based on symptoms, signs or risk factors. NICE recommends testing in people with type 1 diabetes or another autoimmune disease and in new onset atrial fibrillation. Testing can also be considered with depression, unexplained anxiety or menopausal symptoms that could represent thyroid dysfunction. One non specific symptom alone may not justify testing repeatedly. Clinical judgement considers the combination, severity, duration and previous results. Avoid routine testing during acute illness Acute illness can temporarily change TSH, T4 and T3 without true thyroid disease. This is sometimes called non thyroidal illness. NICE advises against thyroid testing during an acute illness unless the illness may be caused by thyroid dysfunction. An abnormal result obtained during severe illness may need repeating after recovery before a lifelong diagnosis is made. This caution does not apply when myxoedema coma or another thyroid emergency is suspected. Treatment should not be delayed when the clinical pattern indicates a life threatening endocrine emergency. TSH is the usual first line test When pituitary disease is not suspected, NICE advises measuring TSH first in adults. If TSH is above the reference range, free T4 should be measured in the same sample. A raised TSH with low FT4 supports overt primary hypothyroidism. A raised TSH with normal FT4 supports subclinical hypothyroidism after persistence is confirmed. TSH can be misleading in pituitary disease, pregnancy, acute illness and with some laboratory interferences. When TSH and FT4 should be ordered together Both TSH and FT4 should be measured initially when secondary thyroid dysfunction is suspected. Clues include a known pituitary disorder, previous pituitary surgery or radiotherapy, visual field symptoms and evidence of several pituitary hormone deficiencies. A low FT4 with an inappropriately normal or low TSH can indicate central hypothyroidism. The pattern requires specialist interpretation because severe illness and medicines can sometimes resemble it. Treatment monitoring in central hypothyroidism relies mainly on FT4 and clinical status rather than targeting TSH. Biotin can distort thyroid tests High dose biotin is present in some hair, skin and nail supplements and in specialist medical treatments. It can interfere with laboratory assays and produce falsely high or low thyroid results, depending on the test method. NICE advises asking about biotin intake when thyroid dysfunction is suspected. Tell the clinician and laboratory about supplements rather than stopping prescribed treatment independently. Unexpected results that do not fit the clinical picture should prompt review of possible assay interference. Thyroid antibodies and imaging TPO antibodies help identify an autoimmune cause when TSH is raised. They are generally measured once rather than followed over time. Antibody concentration is not used to adjust levothyroxine. Ultrasound does not diagnose hypothyroidism and is not routinely required for abnormal thyroid function tests alone. Imaging is used for a palpable nodule, goitre, neck compression or another structural concern. A scan finding and a hormone abnormality answer different clinical questions. Deciding whether to treat subclinical hypothyroidism Treatment depends on persistent TSH elevation, age, symptoms, thyroid antibodies, cardiovascular context and evidence of underlying thyroid disease. NICE advises considering levothyroxine when TSH is 10 milliunits per litre or higher on two occasions three months apart. For adults under 65 with symptoms and TSH above the reference range but below 10 on two tests, a six month levothyroxine trial can be considered. If symptoms persist after TSH normalises, treatment may be stopped and alternative causes reviewed. This approach reduces both undertreatment of significant disease and unnecessary lifelong medication for symptoms unrelated to thyroid function. Monitoring untreated subclinical hypothyroidism Some people do not need immediate medicine. Monitoring checks whether thyroid function normalises, remains stable or progresses. NICE advises considering annual TSH and FT4 testing when features suggest underlying thyroid disease, such as positive antibodies or previous thyroid treatment. Testing every two to three years can be considered when no such features are present. Earlier reassessment is appropriate if symptoms change, pregnancy occurs or a new medicine affects thyroid function. A monitoring decision should be recorded so that mild abnormalities are neither forgotten nor tested excessively. Levothyroxine replaces T4 Levothyroxine is a synthetic form of T4 that is chemically equivalent to the main hormone produced by the thyroid. Body tissues convert it into T3 as needed. Its long half life allows stable once daily dosing. NICE recommends levothyroxine as first line treatment for primary hypothyroidism. The aim is to restore hormone availability, improve symptoms and maintain TSH within the reference range without causing excess. Levothyroxine controls the condition but does not reverse permanent destruction or removal of the thyroid gland. Starting dose in younger adults For adults under 65 without cardiovascular disease, NICE advises considering approximately 1.6 micrograms per kilogram each day, rounded to an appropriate tablet strength. The exact dose is individualised. Body weight, residual thyroid function, pregnancy, absorption and other medicines affect requirements. A person with mild or temporary hypothyroidism may need less than full replacement. The prescription should use micrograms clearly because milligram errors would represent a thousand fold difference. Dose decisions belong to the prescribing clinician and should not be calculated from body weight at home. Older adults and cardiac disease Adults aged 65 or over and people with cardiovascular disease generally begin with a lower dose, commonly 25 to 50 micrograms daily. The dose is increased cautiously according to symptoms and blood tests. Rapid correction can provoke angina, arrhythmia or heart failure in a susceptible person. Starting low does not mean leaving someone permanently undertreated. The dose is titrated towards an appropriate biochemical and clinical target. New chest pain, palpitations, fainting or severe breathlessness during titration requires prompt medical review. How to take levothyroxine Levothyroxine absorption is most predictable when taken consistently on an empty stomach. NHS advice is to take it with water 30 to 60 minutes before breakfast, caffeine or other medicines. Some people use a consistent bedtime schedule well after food when this has been agreed and produces stable tests. The important principle is a repeatable routine rather than alternating between fed and fasting administration. If the routine changes, thyroid function may need reassessment because absorption can change. Food and caffeine Food reduces and delays levothyroxine absorption. Coffee and other caffeinated drinks can also reduce absorption when taken too close to the dose. Milk, soya products and high fibre meals may affect absorption in some people. You do not usually need to avoid these foods completely. Separation and consistency are more practical. A sudden dietary change can alter TSH even when the prescribed dose has not changed. Diet should be reviewed before assuming that persistent abnormal tests require a large dose escalation. Calcium and iron Calcium and iron supplements can bind levothyroxine in the gut and reduce absorption. NHS England advises separating antacids, calcium and iron from levothyroxine by about four hours. Pregnancy supplements commonly contain iron or calcium, making timing especially important. Some multivitamins and indigestion products contain these minerals without the interaction being obvious. A pharmacist can help create a practical schedule that protects both thyroid treatment and necessary supplementation. Proton pump inhibitors and antacids Proton pump inhibitors, including omeprazole, reduce stomach acidity and can alter levothyroxine tablet absorption. Antacids containing aluminium, magnesium or calcium can also interfere. These medicines may be necessary for ulcer prevention, reflux or other gastrointestinal disease. Do not stop gastroprotection independently. A clinician may adjust timing, monitor TSH or consider a different levothyroxine formulation. Persistent unexplained TSH variation should prompt a structured interaction and adherence review before assuming treatment resistance. Other interactions Carbamazepine and some other enzyme inducing medicines can increase thyroid hormone metabolism. Sertraline, bile acid sequestrants and several specialist medicines can alter levothyroxine requirements or absorption. Oestrogen therapy can increase thyroid binding proteins and sometimes increase the required dose. Starting or stopping an interacting medicine can change thyroid control even after years of stability. Tell your clinician and pharmacist about all prescriptions, supplements and over the counter products. Consistency of levothyroxine products Generic levothyroxine prescribing is suitable for most people, and authorised products must meet quality standards. A small minority report symptoms or loss of biochemical control after switching between tablet formulations. MHRA advises checking thyroid function when symptoms follow a switch. If problems persist, a specific product known to be well tolerated can be prescribed consistently. An oral solution may be considered when symptoms or control remain problematic despite consistent use of one tablet product. Missed doses If you forget a dose, NHS advice is to take it when remembered unless it is nearly time for the next dose. If the next dose is close, skip the missed dose and continue normally. Do not take two doses together to compensate. Levothyroxine has a long half life, so one missed dose does not usually cause an immediate crisis. Frequent missed doses can keep TSH raised and lead to inappropriate dose escalation if they are not discussed honestly. A simpler routine, reminder or pharmacist review may improve consistency. Monitoring after starting or changing dose TSH changes slowly because levothyroxine has a long half life and the pituitary needs time to reach a new equilibrium. SPS advises checking TSH from around six weeks after starting treatment or changing the dose. NICE advises measurements every three months until two similar results within range are obtained three months apart, then annually. FT4 can also be checked when symptoms persist despite treatment. Testing too early can lead to repeated dose changes before the previous adjustment has taken full effect. Why six to eight weeks matters Many clinical pathways use a six to eight week interval after a dose change because near steady state hormone levels need several half lives. This interval is a practical minimum rather than a guarantee that severe longstanding hypothyroidism has fully corrected. TSH can take up to six months to normalise after a very high starting value or a prolonged untreated period. Clinicians avoid chasing each early result with large rapid adjustments. Symptoms, adherence, interactions and FT4 provide additional context during this period. The treatment target For primary hypothyroidism, NICE advises aiming for TSH within the laboratory reference range. If symptoms persist, the dose can sometimes be adjusted within that range while avoiding TSH suppression. A suppressed TSH suggests excessive thyroid hormone effect unless specialist treatment intentionally requires suppression. The target is not the lowest possible TSH and does not depend on maximising energy or weight loss. Clinical wellbeing and biochemical safety are considered together. Persistent symptoms despite normal TSH Some people continue to experience fatigue, pain, low mood or cognitive symptoms after TSH normalises. The first step is to confirm adherence, timing, interactions, dose history and the original diagnosis. Anaemia, sleep disorders, menopause, depression, chronic pain and other conditions may explain ongoing symptoms. NICE does not recommend routine liothyronine because evidence of additional benefit is insufficient and long term harms remain uncertain. Selected specialist supervised trials may be considered in exceptional circumstances after a structured review. Liothyronine and desiccated thyroid extract Liothyronine is synthetic T3. It acts more rapidly and produces greater fluctuations than levothyroxine. NICE advises not routinely offering liothyronine alone or with levothyroxine for primary hypothyroidism. Natural or desiccated thyroid extract contains variable proportions of T4 and T3 derived from animal thyroid tissue. NICE advises against natural thyroid extract because benefit over levothyroxine has not been established and long term safety is uncertain. These products should not be started or purchased without specialist clinical oversight. Symptoms of too much levothyroxine Over replacement can cause palpitations, tremor, sweating, anxiety, diarrhoea, heat intolerance, weight loss and insomnia. Some people, particularly older adults, may present mainly with atrial fibrillation, breathlessness or weakness. Symptoms overlap with anxiety, menopause and other disorders, so a blood test is needed. Do not repeatedly reduce or increase the dose according to symptoms alone. Severe chest pain, collapse or a sustained rapid irregular heartbeat requires urgent assessment. Atrial fibrillation risk A persistently suppressed TSH from excessive replacement increases the risk of atrial fibrillation, particularly in older adults. Atrial fibrillation can cause palpitations, breathlessness, dizziness or no obvious symptoms. It increases stroke risk and requires its own assessment and management. The risk is one reason treatment aims for an appropriate reference range TSH rather than deliberate over replacement. New palpitations should prompt pulse assessment, ECG and thyroid testing rather than unsupervised dose changes. Bone effects of over replacement Excess thyroid hormone accelerates bone turnover. Over time, this can reduce bone density and increase fragility fracture risk. Postmenopausal women and people with existing osteoporosis are particularly vulnerable. A short temporary TSH change is not the same as years of sustained over replacement. Regular monitoring identifies excessive dosing before substantial harm develops. Levothyroxine used at the correct replacement dose does not inherently cause osteoporosis. Pregnancy changes thyroid requirements Pregnancy increases thyroid hormone requirements early, often before the first routine antenatal appointment. Oestrogen increases thyroid binding proteins, the placenta handles thyroid hormones and maternal physiology changes. The developing fetus depends on maternal thyroid hormone, particularly early in pregnancy. Untreated or undertreated hypothyroidism increases risks including miscarriage, pre eclampsia, premature birth, low birthweight and impaired fetal development. Levothyroxine is safe and necessary during pregnancy when hypothyroidism is present. What to do when pregnancy is confirmed If you take levothyroxine and become pregnant, contact your GP, midwife or endocrine team promptly. Do not wait for a routine booking visit. Thyroid blood tests should be arranged, and many people require an early dose increase. RCOG states that the body needs more thyroxine during pregnancy and that the dose may need changing as soon as pregnancy is confirmed. The exact increase depends on your current dose, cause of hypothyroidism and recent results. Follow your agreed pre pregnancy plan or urgent clinical advice. Do not stop levothyroxine because of pregnancy or morning sickness without seeking help. Monitoring during pregnancy Pregnancy requires more frequent thyroid testing using pregnancy specific interpretation. A common approach is to repeat testing about four to six weeks after an initial dose change and at intervals through pregnancy. The obstetric and endocrine team adjusts treatment to maintain appropriate trimester related targets. Iron and calcium supplements should be taken separately from levothyroxine because they reduce absorption. After birth, the dose often returns towards the pre pregnancy requirement and thyroid function is rechecked. Planning pregnancy Tell your clinician before trying to conceive so that TSH can be optimised and a pregnancy action plan agreed. Fertility treatment services may use specific thyroid thresholds according to reproductive guidance. A positive TPO antibody result alone does not automatically mean that levothyroxine is needed when TSH and FT4 are normal. Iodine needs increase during pregnancy, but excessive iodine or seaweed supplements can be harmful. Preconception review also ensures that calcium or iron timing will not interfere with replacement therapy. Breastfeeding Levothyroxine is compatible with breastfeeding and supports normal maternal thyroid function. Only very small amounts enter breast milk, and treatment should not be stopped. Postpartum dose requirements can change, especially after a pregnancy related increase. Postpartum thyroiditis can also cause a period of high and then low thyroid function. Follow up testing distinguishes a temporary postpartum change from permanent hypothyroidism. Older adults Symptoms in older adults may be subtle and can resemble frailty, depression, dementia or medicine effects. Severe biochemical hypothyroidism can occur with few classic symptoms. Conversely, mild TSH elevation may reflect age related reference differences. Treatment starts cautiously because the heart and brain may be vulnerable to rapid hormone changes. Overtreatment can cause atrial fibrillation, fractures, weight loss and muscle weakness. Medication review and gradual titration are therefore particularly important. Cardiovascular disease Thyroid hormone increases heart rate, contractility and oxygen demand. Someone with coronary artery disease may develop angina when a large replacement dose is introduced too quickly. Lower starting doses and slower titration allow the cardiovascular system to adapt. This does not justify leaving severe hypothyroidism untreated indefinitely. Cardiac and endocrine risks are balanced together. Acute coronary symptoms require emergency assessment rather than a routine thyroid appointment. Myxoedema coma Myxoedema coma is a rare, life threatening decompensation of severe hypothyroidism. Not everyone is literally comatose at presentation. The key pattern is altered mental state with severe physiological slowing and failure of several body systems. Features can include hypothermia, confusion or reduced consciousness, slow heart rate, low blood pressure, low sodium and respiratory depression. It occurs most often in older people with longstanding untreated or undertreated disease. Immediate hospital and intensive supportive treatment are required. Triggers for myxoedema coma Infection is a common precipitant. Pneumonia, urinary infection or sepsis can overwhelm the body's limited reserve. Cold exposure, trauma, surgery, stroke and heart failure can also trigger decompensation. Sedatives, opioids and other medicines that suppress breathing or consciousness can increase risk. Stopping levothyroxine for a prolonged period may contribute, particularly after total thyroidectomy or radioiodine destruction. The emergency is diagnosed from the whole clinical pattern and treated before every test result returns. Myxoedema coma is not ordinary tiredness Routine fatigue, cold intolerance and constipation do not mean that myxoedema coma is developing. The emergency involves marked deterioration, altered consciousness, hypothermia or unstable breathing and circulation. The term should be explained accurately to avoid alarming people with stable treated hypothyroidism. Calling 999 is appropriate when severe physiological or neurological features are present. Emergency treatment includes thyroid hormone, corticosteroid cover, treatment of the trigger and organ support under specialist care. Is treatment lifelong? Treatment is usually lifelong when hypothyroidism results from Hashimoto's destruction, total thyroidectomy or radioiodine treatment. Some forms of thyroiditis and some mild subclinical abnormalities can recover. The original cause should therefore be documented rather than assuming that every prescription must continue forever. Levothyroxine should not be stopped as an unsupervised experiment because symptoms and biochemical deficiency can return. A planned trial off treatment may be appropriate only when the diagnosis or permanence is uncertain and monitoring is arranged. Long term monitoring Once TSH is stable in primary hypothyroidism, NICE advises annual monitoring for adults. Earlier testing is appropriate after dose, product, pregnancy, weight, adherence or interacting medicine changes. Monitoring is also brought forward when symptoms of under replacement or over replacement appear. Central hypothyroidism requires specialist targets based mainly on FT4 because TSH is unreliable. Regular review prevents both recurrence of hormone deficiency and complications from excessive replacement. The main goal Good hypothyroidism care replaces the hormone your body lacks without creating thyroid excess. It confirms the biochemical pattern, identifies whether the problem is primary or central and considers the underlying cause. It uses a consistent medicine routine, checks for interactions and waits long enough for dose changes to take effect. It responds rapidly to pregnancy, cardiac risk and severe decompensation. It also recognises when persistent symptoms need investigation beyond the thyroid rather than indefinite dose escalation.

Hypothyroidism is diagnosed from the relationship between TSH and free T4, not from symptoms alone. Most primary disease is treated safely with consistent levothyroxine dosing and periodic monitoring, while pregnancy, pituitary disease, cardiac disease and severe decompensation require modified or urgent management.