T3 t4 and tsh relationship questions

Thyroid Gland Overview - A Major Player in Regulating Your Metabolism

t3 t4 and tsh relationship questions

T3 and T4 production is regulated by thyroid stimulating hormone (TSH) is a relationship between serum free T4 and TSH concentrations in that very treat asthma, arthritis, and other health problems, can lower T4 levels. Explore the latest articles, projects, and questions and answers in TSH, and find TSH Has anyone found reliable kits for testing T4,T3,and TSH in rat serum? . What is the relationship between human hormones, such as which one is. This article attempts to explain the problems with interpretation of thyroid of free T4 and free T3 circulating in the blood and adjust the amount of TSH If the pituitary fails to make enough TSH then free T4 levels in the blood.

Association of Depression with Postpartum Thyroid Disease The association of postpartum depression with postpartum thyroiditis or with positive thyroid antibodies is still not well defined. Early studies noted a minor association between thyroid dysfunction and postnatal depression [ 82 ].

More recently, a higher frequency of mild to moderate depression was observed in postpartum female subjects with positive antithyroid antibodies regardless of thyroid function [ 83 — 85 ]. However, an attempt to decrease the incidence of postpartum depression in thyroid antibody positive women with daily administration of thyroxine for 18 weeks postpartum was unsuccessful [ 86 ].

Neuroimaging in Thyroid and Mood Disorders A few studies have been performed to assess the changes in cerebral perfusion and metabolism in patients with hypothyroidism particularly those with Hashimoto's thyroiditis or status post-thyroidectomy for thyroid carcinoma. Some have reported diffuse global hypoperfusion [ 87 — 89 ] while others demonstrated decreased regional cerebral blood flow [ 90 — 92 ]. Furthermore, variable findings regarding restoration of blood flow with treatment have been documented.

While some demonstrated at least partial normalization of cerebral blood flow [ 148789 ] others found persistent hypoperfusion with restoration of the euthyroid state [ 90 — 92 ].

The inconsistency in the above findings can be accounted for by the variability in the degree of hypothyroidism and the differences in the etiology and duration of the disease in the various studied populations.

Studies assessing cerebral blood flow and metabolism in depression are more numerous. The most widely replicated finding from these studies is hypoperfusion in anterior cortical structures [ 9394 ] that was reversible after psychotherapy and pharmacotherapy [ 95 — 97 ]. In addition to frontal hypoperfusion, increased perfusion has been observed in various limbic regions most notably the amygdala [ 93 ].

In a study comparing cerebral blood flow in hypothyroidism and major depression, hypothyroid patients exhibited hypoperfusion in posterior aspects of the brain in contrast to an anterior cerebral hypoperfusion in depressed patients.

Furthermore, normalization of perfusion abnormalities in patients with depression after treatment was observed while no change in cerebral blood flow was noted in hypothyroidism. This implies that behavioral symptoms in depression may be mediated by different neural circuits from that seen in hypothyroidism [ 92 ]. Conclusion Clinical investigators have long recognized the link between thyroid and depression.

While patients with hypothyroidism commonly manifest features of depression, hyperthyroidism presents with a wider spectrum of neuropsychiatric symptoms including both depression and anxiety. On the other hand, most of the patients with primary depression have normal thyroid function. The mechanisms underlying the interaction between thyroid function and depression remain to be clarified and a causal relationship between the two cannot be established yet.

A possible role for thyroid autoimmunity in the pathogenesis of depression can be elucidated. Screening patients presenting with depression for thyroid dysfunction seems reasonable particularly those with refractory symptoms. However, the use of thyroid hormones as an adjunct therapy to antidepressants in the absence of subclinical or clinical hypothyroidism should be further investigated.

t3 t4 and tsh relationship questions

In addition, specifying a particular patient population that might benefit from this combination as determined by individual genetic variants should be addressed. The continuing research in the biochemical, genetic, and neuroimaging fields seems most promising in providing a deeper understanding of the thyroid-depression interactions.

The Scientific Basis of Clinical Practice. Relationships between circulating and intracellular thyroid hormones: Role of transthyretin in the transport of thyroxine from the blood to the choroid plexus, the cerebrospinal fluid, and the brain.

Robbins J, Lakshmanan M. The movement of thyroid hormones in the central nervous system. Thyroid hormone transport in and out of cells. Trends in Endocrinology and Metabolism. Neurodevelopmental and neurophysiological actions of thyroid hormone. American Journal of Psychiatry. The relationship of anxiety and depression to symptoms of hyperthyroidism using operational criteria. Mental changes accompanying thyroid gland dysfunction. A reappraisal using objective psychological measurement. Archives of General Psychiatry.

Prevalence of depression in patients affected by subclinical hypothyroidism. Brain glucose metabolism in hypothyroidism: Journal of Clinical Endocrinology and Metabolism. Basal thyrotropin and major depression: Canadian Journal of Psychiatry. Common variation in the DIO2 gene predicts baseline psychological well-being and response to combination thyroxine plus triiodothyronine therapy in hypothyroid patients. Polymorphisms in the brain-specific thyroid hormone transporter OATP1C1 are associated with fatigue and depression in hypothyroid patients.

American association of clinical endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. The International Encyclopedia of Depression.

t3 t4 and tsh relationship questions

Hormones of the hypothalamic-pituitary-thyroid axis: Hypothalamic-pituitary-thyroid-axis function in treatment resistant depression. Journal of Affective Disorders. Rapid cycling bipolar affective disorder. Association with grade I hypothyroidism. The thyroid axis and depression. Low levels of transthyretin in the CSF of depressed patients. Increased depressive behaviour in mice harboring the mutant thyroid hormone receptor alpha 1.

The Link between Thyroid Function and Depression

Plasma membrane transport of thyroid hormones and its role in thyroid hormone metabolism and bioavailability. CSF transthyretin in patients with depression. Low cerebrospinal fluid transthyretin levels in depression: Suzuki T, Abe T. Thyroid hormone transporters in the brain. Serum thyrotropin in hospitalized psychiatric patients: The relation between thyroid function and depression: Revista Brasileira de Psiquiatria. Antidepressants inhibit the glucocorticoid stimulation of thyrotropin releasing hormone expression in cultured hypothalamic neurons.

Journal of Investigative Medicine. Thyroid function and the natural history of depression: Low T3 syndrome in psychiatric depression. Journal of Endocrinological Investigation. Increased production of thyroxine and inappropriately elevated serum thyrotropin in levels in endogenous depression.

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High reverse T3 levels in manic and unipolar depressed women. Kirkegaard C, Faber J. Altered serum levels of thyroxine, triiodothyronines and diiodothyronines in endogenous depression. Clinical significance of psychoneuroendocrinology in psychiatry: Journal of Clinical Psychiatry.

CSF triiodothyronine rT3 levels in patients with affective disorders. Antithyroid antibodies in depressed patients. Antithyroid antibodies in major depression. The presence of antithyroid antibodies in patients with affective and nonaffective psychiatric disorders. Thyroid function in clinical subtypes of major depression: Circadian rhythm disturbances in depression: Twenty-four-hour profiles of body temperature and plasma TSH in bipolar patients during depression and during remission and in normal control subjects.

t3 t4 and tsh relationship questions

Sensitive assay of thyroid stimulating hormone in depressed patients. Effects of thyrotropin-releasing hormone in depression. Improvement in mental depression with decreased thyrotropin response after administration of thyrotropin-releasing hormone. Thyrotropin-releasing hormone TRHthe thyroid axis, and affective disorder. Annals of the New York Academy of Sciences. Serum thyrotropin response to thyrotropin-releasing hormone in psychiatric patients: The thyrotropin response to thyrotropin-releasing hormone in endogenous depression.

Thyrotropin-releasing hormone regulates the number of its own receptors in the GH3 strain of pituitary cells in culture. Dose-response studies with protirelin. Increased levels of TRH in cerebrospinal fluid from patients with endogenous depression. Thyroid axis activity and serotonin function in major depressive episode. Thyrotropin-releasing hormone receptor 1-deficient mice display increased depression and anxiety-like behavior. Enhancement of imipramine antidepressant activity by thyroid hormone.

Potentiation of amitriptyline by thyroid hormone. Thyroid-hormone enhancement of imipramine in nonretarded depressions. New England Journal of Medicine. The comparative antidepressant value of L-tryptophan and imipramine with and without attempted potentiation by liothyronine. Does thyroid supplementation accelerate tricyclic antidepressant response?

t3 t4 and tsh relationship questions

A review and meta-analysis of the literature. Triiodothyronine augmentation in the treatment of refractory depression: Simultaneous initiation coinitiation of pharmacotherapy with triiodothyronine and a selective serotonin reuptake inhibitor for major depressive disorder: Preliminary evidence that a functional polymorphism in type 1 deiodinase is associated with enhanced potentiation of the antidepressant effect of sertraline by triiodothyronine.

Joffe RT, Singer W. A comparison of triiodothyronine and thyroxine in the potentiation of tricyclic antidepressants. Thyroxine and the treatment of affective disorders: International Journal of Neuropsychopharmacology. Supraphysiological doses of L-Thyroxine in the maintenance treatment of prophylaxis-resistant affective disorders. The thyroid-brain interaction in thyroid disorders and mood disorders.

The effect of tricyclic antidepressants on basal thyroid hormone levels in depressed patients. Low plasma thyroid indices of depressed patients are attenuated by antidepressant drugs and influence treatment outcome. The influence of desipramine on thyroid hormone metabolism in rat brain. Journal of Pharmacology and Experimental Therapeutics. Subchronic administration of fluoxetine to rats affects triiodothyronine production and deiodination in regions of the cortex and in the limbic forebrain.

A hypothesis of thyroid-catecholamine-receptor interaction. Its relevance to affective illness. American Journal of Nursing. If the pituitary fails to make enough TSH then free T4 levels in the blood will fall — but since the problem is at pituitary level then TSH levels in the blood do not rise appropriately.

t3 t4 and tsh relationship questions

In severe cases free T4 will fall below the normal range, while TSH levels can be normal or low see diagram. If the patient then receives levothyroxine replacement for their thyroid the free T4 levels will rise, and TSH levels often fall to below normal. This means that TSH levels alone are useless for deciding whether someone with pituitary disease has developed a pituitary-thyroid deficiency or whether they are on the correct amount of levothyroxine replacement or too much or too little.

Endocrinologists are aware of this problem, and will usually always request a free T4 measurement from the laboratory in patients with pituitary disease. In my experience, this often leads to inappropriate reductions in levothyroxine dosage by the primary care team — when a low TSH level is interpreted as a sign of too much levothyroxine which is true in people with thyroid problems rather than as simply a sign of the pituitary deficiency which is being treated.

However, even endocrinologists have problems knowing exactly what a lowish free T4 level means because of the wide range of free T4 in normal people. A common dilemma is whether a level in the lower part of the normal range represents a deficiency for someone who would run in the higher part of normal if nothing was wrong with their pituitary or is simply the normal level at which that person has always been.

Equally, when a decision has been made to start levothyroxine replacement it is difficult to know exactly what free T4 level to aim for. There are potential risks from giving too much or too little levothyroxine so ideally we would like to get things as normal as possible. In order to find out more about this, we reviewed the results of thyroid blood tests in all patients with pituitary tumours in our department and we have recently published the results in the UK medical journal Clinical Endocrinology.

We looked at results of tests in over pituitary patients, almost of whom were taking levothyroxine — and we compared the levels we found with over 20, sets of thyroid blood tests in patients with problems with the thyroid gland itself who had a normal pituitary. We were pleased to find that we had indeed measured free T4 levels in almost everyone, and that very few people had levels outside the normal range.

However, we were less pleased to discover that many more patients with pituitary disease had levels of free T4 in the lower part of normal when compared to patients we were treating with thyroid disease. Overall we suggested that this means that we are probably failing to diagnose and treat mild levels of pituitary-thyroid TSH deficiency in some of our patients, and that we are not giving many of our pituitary patients enough levothyroxine to keep free T4 levels up to the range which we know represents optimal replacement in people with a normal pituitary.

We suspect that the same thing will be happening in many other places. We were able to do this study because we have collected details on diagnosis and treatment of all our patients in a clinical database for over 20 years and therefore have detailed information on large numbers of patients with pituitary disease and thyroid disease, with all the thyroid blood tests checked in a single hospital laboratory and available for comparison.

Most other places would not be able to pull together all this information to compare results in their centre — but if they could we think it is likely they would find the same thing.