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So, what's the scoop. I know at least a decade ago it was being done. Is it still used? Any good studies negating/advocating for it?
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Cytomel as Depression adjunct
- Thread starter Sneezing
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There was a great article in Current Psychiatry about 2 years ago that dealt with using thyroid hormones as an augmentation agent in depression. Do you have membership with CP?
Also, I do believe it was in the STAR*D trial. While I read it, I usually use Buspirone as a first augmentation agent because most of the patients I have with treatment resistant depression have comorbid anxiety, so I don't have much experience with cytomel.
Also, I do believe it was in the STAR*D trial. While I read it, I usually use Buspirone as a first augmentation agent because most of the patients I have with treatment resistant depression have comorbid anxiety, so I don't have much experience with cytomel.
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I did a quick MDConsult/Medline search for journal articles from 2004-current for the terms "depression, t3, t4" and got 386 results. I sorted by "relevance" and looked at the first 140 article titles (b/c by then none were "relevant", and then looked at the abstracts of those that looked promising.
To answer your question: My guess from my education, VERY limited experience with this particular issue, and reading previous posts on SDN about this; is that there probably is no real answer, but some people have strong feelings one way or the other. Personally, I would start with thyroxine as a thyroid aug. strategy (though I'd probably try other aug strategies first), and if getting partial response, I would then try switching to T3.
To other frequent posters: I could sure use some input here.
PARTICULARLY INTERESTING:
They also emphasize the large and sustained placebo effect that can follow changes in thyroid hormone administration. ( J Clin Endocrinol Metab 90: 805812, 2005)
Does substitution of T4 with T3 plus T4 for T4 replacement improve depressive symptoms in patients with hypothyroidism? - Joffe RT - Ann N Y Acad Sci - 01-DEC-2004; 1032: 287-8
Substitution of T4 with T3 for T4 replacement in patients with hypothyroidism was undertaken using a randomized placebo controlled study design. Forty individuals were included who had depressive symptoms on stable doses of levothyroxine. Combined T4 plus T3 did not have a significantly different effect on mood and well-being scores than did T4 alone.
Therapeutic options for treatment-resistant depression. - Shelton RC - CNS Drugs - 1-FEB-2010; 24(2): 131-61
In summary, despite an increasing variety of choices for the treatment of TRD, this condition remains universally undefined and represents an area of unmet medical need. There are few known approved pharmacological agents for TRD (aripiprazole and OFC) and overall outcomes remain poor. This might be an indication that depression itself is a heterogeneous condition with a great diversity of pathologies, highlighting the need for careful evaluation of individuals with depressive symptoms who are unresponsive to treatment. Clearly, more research is needed to provide clinicians with better guidance in making those treatment decisions--especially in light of accumulating evidence that the longer patients are unsuccessfully treated, the worse their long-term prognosis tends to be.
Effect of combination therapy with thyroxine (T4) and 3,5,3'-triiodothyronine versus T4 monotherapy in patients with hypothyroidism, a double-blind, randomised cross-over study. - Nygaard B - Eur J Endocrinol - 01-DEC-2009; 161(6): 895-902
CONCLUSION: In a study design, where morning TSH levels were unaltered between groups combination therapy, (treated with T(3) 20 microg once daily) was superior to monotherapy by evaluating several QOL, depression and anxiety rating scales as well as patients own preference.
Efficacy and safety of triiodothyronine supplementation in patients with major depressive disorder treated with specific serotonin reuptake inhibitors. - Cooper-Kazaz R - Int J Neuropsychopharmacol - 01-AUG-2008; 11(5): 685-99
The RCTs were too disparate in methodology to allow a meta-analysis to be performed. The enhancement studies are inconclusive in that one showed strongly positive effects of T3, one showed no effect and one showed a trend. The open augmentation studies supported an effect of T3 in SSRI non-responsive patients with some support from a large RCT; a smaller, underpowered RCT did not show efficacy. T3 was well tolerated in most of the studies and adverse effects do not seem to be an impediment to clinical use. Some of the studies identified clinical and thyroid function correlates of response that require further investigation. Further research is needed before it can be definitively established whether T3 is an effective supplement to SSRIs in patients with MDD. The appropriate timing of T3 supplementation needs to be explored and also the dose and length of treatment.
[Potentializing of tricyclics and serotoninergics by thyroid hormones in resistant depressive disorders] - Sintzel F - Encephale - 01-MAY-2004; 30(3): 267-75
On the basis of numerous studies carried out on the potentializing of tricyclics, we suggest practical modalities of treatment - which until today did not materialize in every day practice in the absence of a clear consensus based on statistically reliable data: after four to six weeks of inefficient tricyclic or serotoninergic treatment on a correct dosage testified by plasmatic dosages, it is recommended to initiate a T3 treatment on a effective posology (25 to 50 micrograms per day), which must be reached in 2 or 3 days, except in case of rare and transitory side effects (sweating, shaking, tachycardia, nervousness, anxiety). If the treatment is not rapidly efficient, it must be discontinued in case there is no improvement after 3 weeks. Until today, there is no consensus about the duration of a T3 treatment. It is important to take into account the predictive criteria of good or bad response to a T3 potentialization, since they have direct consequences on the management of depressed patients. For example, a high degree of chronic evolution with resistance to numerous treatments, associated disorders according to the DSM IV axis I and a comorbidity of addiction, point to a bad prognosis of a potentialization treatment. In addition, we'll examine the few recent studies on the potentializing of serotoninergic antidepressant drugs by thyroid hormones.
L-thyroxine augmentation of serotonergic antidepressants in female patients with refractory depression. - Łojko D - J Affect Disord - 01-NOV-2007; 103(1-3): 253-6
CONCLUSIONS: The addition of moderate dose of l-thyroxine may be a successful augmentation strategy in female depressed patients in whom the effect of serotonergic antidepressant had been unsatisfactory. It may be efficient despite of the lack of disturbances of thyroid axis in such patients.
Preliminary evidence that a functional polymorphism in type 1 deiodinase is associated with enhanced potentiation of the antidepressant effect of sertraline by triiodothyronine. - Cooper-Kazaz R - J Affect Disord - 01-JUL-2009; 116(1-2): 113-6
DISCUSSION: DIO1 plays a key-role in T4 to T3 conversion and in clearance of the inactive metabolite, rT3. Previous data associate the DIO1-785T allele with lower DIO1 activity. This is consistent with our observation that responders to T3 supplementation had lower baseline serum T3 levels than non-responders. Depressed patients, who have a genetically determined lower T4 to T3 conversion, may be more likely to benefit from T3 supplementation.
To answer your question: My guess from my education, VERY limited experience with this particular issue, and reading previous posts on SDN about this; is that there probably is no real answer, but some people have strong feelings one way or the other. Personally, I would start with thyroxine as a thyroid aug. strategy (though I'd probably try other aug strategies first), and if getting partial response, I would then try switching to T3.
To other frequent posters: I could sure use some input here.
PARTICULARLY INTERESTING:
They also emphasize the large and sustained placebo effect that can follow changes in thyroid hormone administration. ( J Clin Endocrinol Metab 90: 805812, 2005)
Does substitution of T4 with T3 plus T4 for T4 replacement improve depressive symptoms in patients with hypothyroidism? - Joffe RT - Ann N Y Acad Sci - 01-DEC-2004; 1032: 287-8
Substitution of T4 with T3 for T4 replacement in patients with hypothyroidism was undertaken using a randomized placebo controlled study design. Forty individuals were included who had depressive symptoms on stable doses of levothyroxine. Combined T4 plus T3 did not have a significantly different effect on mood and well-being scores than did T4 alone.
Therapeutic options for treatment-resistant depression. - Shelton RC - CNS Drugs - 1-FEB-2010; 24(2): 131-61
In summary, despite an increasing variety of choices for the treatment of TRD, this condition remains universally undefined and represents an area of unmet medical need. There are few known approved pharmacological agents for TRD (aripiprazole and OFC) and overall outcomes remain poor. This might be an indication that depression itself is a heterogeneous condition with a great diversity of pathologies, highlighting the need for careful evaluation of individuals with depressive symptoms who are unresponsive to treatment. Clearly, more research is needed to provide clinicians with better guidance in making those treatment decisions--especially in light of accumulating evidence that the longer patients are unsuccessfully treated, the worse their long-term prognosis tends to be.
Effect of combination therapy with thyroxine (T4) and 3,5,3'-triiodothyronine versus T4 monotherapy in patients with hypothyroidism, a double-blind, randomised cross-over study. - Nygaard B - Eur J Endocrinol - 01-DEC-2009; 161(6): 895-902
CONCLUSION: In a study design, where morning TSH levels were unaltered between groups combination therapy, (treated with T(3) 20 microg once daily) was superior to monotherapy by evaluating several QOL, depression and anxiety rating scales as well as patients own preference.
Efficacy and safety of triiodothyronine supplementation in patients with major depressive disorder treated with specific serotonin reuptake inhibitors. - Cooper-Kazaz R - Int J Neuropsychopharmacol - 01-AUG-2008; 11(5): 685-99
The RCTs were too disparate in methodology to allow a meta-analysis to be performed. The enhancement studies are inconclusive in that one showed strongly positive effects of T3, one showed no effect and one showed a trend. The open augmentation studies supported an effect of T3 in SSRI non-responsive patients with some support from a large RCT; a smaller, underpowered RCT did not show efficacy. T3 was well tolerated in most of the studies and adverse effects do not seem to be an impediment to clinical use. Some of the studies identified clinical and thyroid function correlates of response that require further investigation. Further research is needed before it can be definitively established whether T3 is an effective supplement to SSRIs in patients with MDD. The appropriate timing of T3 supplementation needs to be explored and also the dose and length of treatment.
[Potentializing of tricyclics and serotoninergics by thyroid hormones in resistant depressive disorders] - Sintzel F - Encephale - 01-MAY-2004; 30(3): 267-75
On the basis of numerous studies carried out on the potentializing of tricyclics, we suggest practical modalities of treatment - which until today did not materialize in every day practice in the absence of a clear consensus based on statistically reliable data: after four to six weeks of inefficient tricyclic or serotoninergic treatment on a correct dosage testified by plasmatic dosages, it is recommended to initiate a T3 treatment on a effective posology (25 to 50 micrograms per day), which must be reached in 2 or 3 days, except in case of rare and transitory side effects (sweating, shaking, tachycardia, nervousness, anxiety). If the treatment is not rapidly efficient, it must be discontinued in case there is no improvement after 3 weeks. Until today, there is no consensus about the duration of a T3 treatment. It is important to take into account the predictive criteria of good or bad response to a T3 potentialization, since they have direct consequences on the management of depressed patients. For example, a high degree of chronic evolution with resistance to numerous treatments, associated disorders according to the DSM IV axis I and a comorbidity of addiction, point to a bad prognosis of a potentialization treatment. In addition, we'll examine the few recent studies on the potentializing of serotoninergic antidepressant drugs by thyroid hormones.
L-thyroxine augmentation of serotonergic antidepressants in female patients with refractory depression. - Łojko D - J Affect Disord - 01-NOV-2007; 103(1-3): 253-6
CONCLUSIONS: The addition of moderate dose of l-thyroxine may be a successful augmentation strategy in female depressed patients in whom the effect of serotonergic antidepressant had been unsatisfactory. It may be efficient despite of the lack of disturbances of thyroid axis in such patients.
Preliminary evidence that a functional polymorphism in type 1 deiodinase is associated with enhanced potentiation of the antidepressant effect of sertraline by triiodothyronine. - Cooper-Kazaz R - J Affect Disord - 01-JUL-2009; 116(1-2): 113-6
DISCUSSION: DIO1 plays a key-role in T4 to T3 conversion and in clearance of the inactive metabolite, rT3. Previous data associate the DIO1-785T allele with lower DIO1 activity. This is consistent with our observation that responders to T3 supplementation had lower baseline serum T3 levels than non-responders. Depressed patients, who have a genetically determined lower T4 to T3 conversion, may be more likely to benefit from T3 supplementation.
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