Lingering Psychiatric Symptoms May be Due to Hyperthyroidism
An article in Current Psychiatry Online focusing on hyperthyroidism discusses the possible pituitary/thyroid involvement in some patients who may have a variety of psychiatric symptoms and suggests a thorough pituitary/thyroid work-up be done on psychiatric patients.
Symptoms of hyperthyroidism can mimic those of schizophrenia and bipolar disorder. Psychiatric symptoms can include psychosis, paranoia, anxiety, social withdrawal, intrusive thoughts of violence or bizarre sexual ideation, cognitive impairment, apathy, depression, mania, irritability and emotional lability. Patients can have subclinical (low level) hyperthyroidism co-existing with the psychiatric conditions or vice-versa. Lithium can be helpful for some patients with mood problems co-existing with subclinical hyperthyroidism.
The article warns that even after effective treatment for the hyperthyroid condition, residual psychiatric symptoms can persist for years. These residual psychiatric conditions must be treated as well, and if the cause of the hyperthyroidism is Graves disease, the patient must be provided with a smoking cessation program, since smoking can exacerbate this auto-immune illness.
Blood tests for hyperthyroidism (hypothyroidsim as well) include measurements of serum thyroid-stimulating hormone (TSH), free triiodothyronine (T3) and free levothyroxine (T4).
Read the article: Identifying hyperthyroidism’s psychiatric presentations (December 2006 edition of Current Psychiatry Online)
Read the companion article on hypothyroidism:
Identifying hypothyroidism’s psychiatric presentations (November 2006 edition of Current Psychiatry Online)
Other articles about pituitary and thyroid involvement in schizophrenia:
Hypothyroidism and Psychiatric Illness
Protein Biomarkers for Schizophrenia Studied in Cerebrospinal Fluid
Prenatal Infection Increases Risk of Schizophrenia
Causes of Schizophrenia
Pituitary Volume Shows Psychosis Risk
Posted by Jeanie Wolfson at December 1, 2006 11:00 AM
More Information on
Schizophrenia Symptoms
See also companion article on hypothyroidism and psychiatric presentation
http://www.currentpsychiatry.com/article_pages.asp?AID=4545&UID=
Posted by: Tim at December 1, 2006 12:28 PM
Tim!!! THANK YOU for that link!!! That article talks about the importance of testing more than just TSH when a person has "psychiatric" symptoms!! And when the low thyroid is missed in CHILDREN, it can have a devastating PERMANENT affect on the child's developing brain - such as lowering IQ! So many people, even with classic hypothyroid symptoms get only TSH checked instead of actual thyroid levels, and it gets missed.
You know - even thinking about the Florida jails filled with "mentally ill"... I wonder how many of them also have low or high thyroid levels which may be exacerbating or even causing some of their symptoms. Gee - the courts won't know till they get to the hospitals and get tested.
Posted by: Naomi at December 1, 2006 02:02 PM
Also consider the recent finding of lowered transthyretin in the CSF of schizophrenia patients:
http://www.schizophreniaforum.org/new/detail.asp?id=1303
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quote:
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Transthyretin less abundant in the CSF of schizophrenics
In contrast to the upregulation of VGF, the authors found that three peptides from the protein transthyretin were significantly less abundant in the CSF of schizophrenics. Transthyretin is a thyroid hormone-binding protein that transports thyroxine from the bloodstream to the brain (see Schreiber, 2002). The lower levels of the peptides in schizophrenia could not be explained by demographic variables, according to the authors. A possible effect of cannabis use as detected by urine-positive drug screen was ruled out after a two-way ANOVA analysis found no correlation.
Blood transthyretin, largely derived from the liver, contributes to the supply of brain transthyretin. Huang and colleagues also found a significant decrease in serum transthyretin levels; however, they note that no correlation was detected between absolute levels in CSF and those in serum (in opposition to the results of Reiber, 2001), “suggesting that the liver-derived transthyretin may not contribute to the downregulation in CSF.”
As with VGF, postmortem brain studies supported the SELDI mass spectrometry results. The authors found a 40 percent downregulation of transthyretin levels in postmortem prefrontal cortex from patients with schizophrenia by Western blot.
Citing evidence linking transthyretin to the pathophysiology of schizophrenia and other psychiatric diseases, Huang and colleagues note that the reduced levels of transthyretin in the CSF, serum, and brains of schizophrenia patients suggest a lower level of thyroxine transport. “It is noteworthy that thyroid dysfunction is relatively common in patients with schizophrenia (Morley and Shafer, 1982; Ryan et al., 1994) and indeed with other psychiatric disorders (Kirkegaard and Faber, 1998), possibly genetically linked to the disorders. In addition, in patients with severe forms of both hypo- and hyperthyroidism, psychotic symptoms may occur, and the clinical picture frequently resembles that of schizophrenia (Hall et al., 1986, see ref. below), which may imply that an increase in central nervous system thyroxine function may be linked, the authors write. They also point out that long-term administration of clozapine has been implicated in enhancing central nervous system thyroxine function (Chen and Chen, 2007). (In another recent paper, Wan and colleagues [2006] report alterations similar to those seen by Huang and colleagues, though in a tetramer of transthyretin and in response to treatment with the first-generation antipsychotic chlorpromazine.)
To validate their results, the researchers replicated the SELDI mass spectrometry experiments with a second sample of 17 first-onset, drug-naïve schizophrenia patients and 40 demographically matched healthy volunteers, with similar results. “This suggests that these identified alterations in CSF proteins and peptides are a consistent finding and thus may reflect genuinely the early pathophysiology of schizophrenia.” They report that the sensitivity of the overall profile of peptide changes to distinguish schizophrenia from control samples is 80 percent and 88 percent for the original and replication samples, respectively; the sensitivity was found to be 95 percent in both samples.
Posted by: CopperKettle at December 1, 2006 04:05 PM
Thanks CopperKettle! That is GREAT stuff, linking problems seen in many back to a potential test of CSF and transthyretin...
This is complicated and underscores the fact that many forms (if not all) of schizophrenia needs to be in the realm of MEDICAL care - a neuroendocrine disorder. I am glad that this progress is being made, but I know that the "MENTAL" label is hindering progress translating into actual patient care.
Posted by: Naomi at December 1, 2006 04:41 PM
See also companion article on hypothyroidism and psychiatric presentation
http://www.currentpsychiatry.com/article_pages.asp?AID=4545&UID=
Posted by: Tim at December 1, 2006 12:28 PM
Tim!!! THANK YOU for that link!!! That article talks about the importance of testing more than just TSH when a person has "psychiatric" symptoms!! And when the low thyroid is missed in CHILDREN, it can have a devastating PERMANENT affect on the child's developing brain - such as lowering IQ! So many people, even with classic hypothyroid symptoms get only TSH checked instead of actual thyroid levels, and it gets missed.
You know - even thinking about the Florida jails filled with "mentally ill"... I wonder how many of them also have low or high thyroid levels which may be exacerbating or even causing some of their symptoms. Gee - the courts won't know till they get to the hospitals and get tested.
Posted by: Naomi at December 1, 2006 02:02 PM
Also consider the recent finding of lowered transthyretin in the CSF of schizophrenia patients:
http://www.schizophreniaforum.org/new/detail.asp?id=1303
=======================
quote:
=======================
Transthyretin less abundant in the CSF of schizophrenics
In contrast to the upregulation of VGF, the authors found that three peptides from the protein transthyretin were significantly less abundant in the CSF of schizophrenics. Transthyretin is a thyroid hormone-binding protein that transports thyroxine from the bloodstream to the brain (see Schreiber, 2002). The lower levels of the peptides in schizophrenia could not be explained by demographic variables, according to the authors. A possible effect of cannabis use as detected by urine-positive drug screen was ruled out after a two-way ANOVA analysis found no correlation.
Blood transthyretin, largely derived from the liver, contributes to the supply of brain transthyretin. Huang and colleagues also found a significant decrease in serum transthyretin levels; however, they note that no correlation was detected between absolute levels in CSF and those in serum (in opposition to the results of Reiber, 2001), “suggesting that the liver-derived transthyretin may not contribute to the downregulation in CSF.”
As with VGF, postmortem brain studies supported the SELDI mass spectrometry results. The authors found a 40 percent downregulation of transthyretin levels in postmortem prefrontal cortex from patients with schizophrenia by Western blot.
Citing evidence linking transthyretin to the pathophysiology of schizophrenia and other psychiatric diseases, Huang and colleagues note that the reduced levels of transthyretin in the CSF, serum, and brains of schizophrenia patients suggest a lower level of thyroxine transport. “It is noteworthy that thyroid dysfunction is relatively common in patients with schizophrenia (Morley and Shafer, 1982; Ryan et al., 1994) and indeed with other psychiatric disorders (Kirkegaard and Faber, 1998), possibly genetically linked to the disorders. In addition, in patients with severe forms of both hypo- and hyperthyroidism, psychotic symptoms may occur, and the clinical picture frequently resembles that of schizophrenia (Hall et al., 1986, see ref. below), which may imply that an increase in central nervous system thyroxine function may be linked, the authors write. They also point out that long-term administration of clozapine has been implicated in enhancing central nervous system thyroxine function (Chen and Chen, 2007). (In another recent paper, Wan and colleagues [2006] report alterations similar to those seen by Huang and colleagues, though in a tetramer of transthyretin and in response to treatment with the first-generation antipsychotic chlorpromazine.)
To validate their results, the researchers replicated the SELDI mass spectrometry experiments with a second sample of 17 first-onset, drug-naïve schizophrenia patients and 40 demographically matched healthy volunteers, with similar results. “This suggests that these identified alterations in CSF proteins and peptides are a consistent finding and thus may reflect genuinely the early pathophysiology of schizophrenia.” They report that the sensitivity of the overall profile of peptide changes to distinguish schizophrenia from control samples is 80 percent and 88 percent for the original and replication samples, respectively; the sensitivity was found to be 95 percent in both samples.
Posted by: CopperKettle at December 1, 2006 04:05 PM
Thanks CopperKettle! That is GREAT stuff, linking problems seen in many back to a potential test of CSF and transthyretin...
This is complicated and underscores the fact that many forms (if not all) of schizophrenia needs to be in the realm of MEDICAL care - a neuroendocrine disorder. I am glad that this progress is being made, but I know that the "MENTAL" label is hindering progress translating into actual patient care.
Posted by: Naomi at December 1, 2006 04:41 PM