Borderline Hypothyroidism and Depression

Haggerty, John J.; Prange, Arthur J.

doi:10.1146/annurev.med.46.1.37

Cited by 129 publications

(67 citation statements)

References 31 publications

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“…29, 45 Among the factors that predict response of lipid levels to levothyroxine therapy are higher levels of TSH, insulin resistance, higher levels of pretherapy cholesterol, and type III hyperlipidemia. Some evidence suggests that mild thyroid failure can aggravate bipolar disorder and depression 46 and that it is associated with abnormalities of muscle function, nerve conduction, cardiac function, 47 and cognitive and psychological function, with improvement after levothyroxine therapy. 45,[47][48][49][50] …”

Section: Serum Tsh Concentration Greater Than 10 Miu/lmentioning

confidence: 99%

Subclinical Hypothyroidism: An Update for Primary Care Physicians

Fatourechi

2009

Mayo Clinic Proceedings

294

186

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Subclinical hypothyroidism (SCH), also called mild thyroid failure, is diagnosed when peripheral thyroid hormone levels are within normal reference laboratory range but serum thyroid-stimulating hormone (TSH) levels are mildly elevated. This condition occurs in 3% to 8% of the general population. It is more common in women than men, and its prevalence increases with age. Of patients with SCH, 80% have a serum TSH of less than 10 mIU/L. The most important implication of SCH is high likelihood of progression to clinical hypothyroidism. The possibility that it is a cardiovascular risk factor has been a subject of debate. Large-scale randomized studies are needed for evidence-based recommendations regarding screening for mild thyroid failure and levothyroxine therapy for this condition. Currently, the practical approach is routine levothyroxine therapy for persons with a persistent serum TSH of more than 10.0 mIU/L and individualized therapy for those with a TSH of less than 10.0 mIU/L. © 2009 Mayo Foundation for Medical Education and ResearchOn completion of this article you should be able to: (1) S ubclinical hypothyroidism (SCH) is defined as a serum thyroid-stimulating hormone (TSH) level above the upper limit of normal despite normal levels of serum free thyroxine. 1 Serum TSH has a log-linear relationship with circulating thyroid hormone levels (a 2-fold change in free thyroxine will produce a 100-fold change in TSH). Thus, serum TSH measurement is the necessary test for diagnosis of mild thyroid failure when the peripheral thyroid hormone levels are within normal laboratory range. 1 The individual range for peripheral thyroid hormones is narrower than the population reference laboratory range; therefore, a slight reduction within the normal range will result in elevation of serum TSH above the normal range.Subclinical hypothyroidism or mild thyroid failure is a common problem, with a prevalence of 3% to 8% in the population without known thyroid disease. 2,3 The prevalence increases with age and is higher in women. 2 After the sixth decade of life, the prevalence in men approaches that of women, with a combined prevalence of 10%. 2 Antithyroid antibodies can be detected in 80% of patients with SCH, and 80% of patients with SCH have a serum TSH of less than 10 mIU/L.Before diagnosis of SCH, other causes of an elevated TSH level, such as recovery from nonthyroidal illness, assay variability, presence of heterophile antibodies interfering with the TSH assay, and certain cases of central hypothyroidism with biologically inactive TSH and thyroid hormone resistance, should be excluded. However, the most common cause of elevated TSH is autoimmune thyroid disease. 1 Previous radioiodine therapy, thyroid surgery, and external radiation therapy can also result in mild thyroid failure. Transient SCH may occur after episodes of postpartum, silent, and granulomatous thyroiditis. 1,4 The clinical importance of and therapy for mild elevation of serum TSH (<10 mIU/L) 5 and the exact upper limit of normal for the serum TSH ...

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Section: Serum Tsh Concentration Greater Than 10 Miu/lmentioning

confidence: 99%

Subclinical Hypothyroidism: An Update for Primary Care Physicians

Fatourechi

2009

Mayo Clinic Proceedings

294

186

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“…Furthermore, there is ample evidence to associate thyroid dysfunction with mood disorders. Indeed, one of the most obvious symptoms of overt hypothyroidism is affective disturbance, and abnormal thyroid activity, particularly subclinical hypothyroidism, is present in a disproportionately large number of patients with affective disorder (Haggerty and Prange 1995). Additionally, there is some evidence that depressed patients with either hypothyroidism and/or an antithyroid autoimmune response may be less responsive to antidepressant treatment.…”

Section: Do Thyroid Hormones Also Exert Neurotrophic Effects?mentioning

confidence: 99%

Enhancing neuronal plasticity and cellular resilience to develop novel, improved therapeutics for Difficult-to-Treat depression

Manji

Quiróz

Sporn

et al. 2003

Biological Psychiatry

445

259

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“…201 The clinical efficacy of adjunctive thyroxine (T4) or triiodothyronine (T3) in the treatment of refractory unipolar and bipolar mood disorders has been fairly well established. 202 Cole et al 203 observed in patients with bipolar depression that lower pretreatment thyroid activity (albeit within the normal range) predicted a worse response to treatment.…”

Section: Thyroid Hormone: Neurotrophic Effects In Critical Affective mentioning

confidence: 99%

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Carlson¹,

Singh²,

Zarate³

et al. 2006

NeuroRX

136

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Summary:Major depressive disorder and bipolar disorder are severe mood disorders that affect the lives and functioning of millions each year. The majority of previous neurobiological research and standard pharmacotherapy regimens have approached these illnesses as purely neurochemical disorders, with particular focus on the monoaminergic neurotransmitter systems. Not altogether surprisingly, these treatments are inadequate for many individuals afflicted with these devastating illnesses. Recent advances in functional brain imaging have identified critical neural circuits involving the amygdala and other limbic structures, prefrontal cortical regions, thalamus, and basal ganglia that modulate emotional behavior and are disturbed in primary and secondary mood disorders. Growing evidence suggests that mechanisms of neural plasticity and cellular resilience, including impairments of neurotrophic signaling cascades as well as altered glutamatergic and glucocorticoid signaling, underlie the dysregulation in these circuits. The increasing ability to monitor and modulate activity in these circuits is beginning to yield greater insight into the neurobiological basis of mood disorders. Modulation of dysregulated activity in these affective circuits via pharmacological agents that enhance neuronal resilience and plasticity, and possibly via emerging nonpharmacologic, circuitry-based modalities (for example, deep brain stimulation, magnetic stimulation, or vagus nerve stimulation) offers promising targets for novel experimental therapeutics in the treatment of mood disorders.

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Borderline Hypothyroidism and Depression

Abstract: This review defines subclinical hypothyroidism and examines its influence on the occurrence and course of major depression. Recommendations are presented for the identification and treatment of patients with coexisting mood disorders and borderline thyroid failure.

Cited by 129 publications

References 31 publications

Subclinical Hypothyroidism: An Update for Primary Care Physicians

Subclinical Hypothyroidism: An Update for Primary Care Physicians

Enhancing neuronal plasticity and cellular resilience to develop novel, improved therapeutics for Difficult-to-Treat depression

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

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